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Nossa retina invertida: mal-projetada?

Proponentes da evolução com frequência apontam que a retina de invertebrados é uma característica que indica que esta não foi projetada (por Deus) por causa de sua alocação dentro dos olhos, aparentemente não posicionada da forma mais ideal. Eles referem ao fato de que, para a luz alcançar os fotorreceptores ela tem de passar por todo aparato neural da retina, e presumem que consequente degradação da imagem, formada à altura dos fotorreceptores  ocorre. Em linguagem biológica este arranjo da retina é dito ser invertido porque as células visuais são orientadas de maneira que seus terminais sensoriais são direcionadas para o lado oposto de onde a luz chega. É típico dos vertebrados, mas raros entre invertebrados, sendo encontrado em certos moluscos e aracnídeos.

 

Como de costume, evolucionistas amam apontar para isso como uma evidência de “bad design”, portanto, sendo aparentemente mais condizente com uma explicação naturalista, não-guiada por um Ser inteligente. Dawkins, embora admita que que essa posição da renita e toda a travessia da luz até os fotorreceptores não interfira significantemente na qualidade da imagem, escrevera o seguinte:

 

‘Qualquer engenheiro naturalmente esperaria que os fotorreceptores apontassem em direção a luz, e suas ligações (nervosas) em direção ao cérebro. Ele gargalharia diante de qualquer sugestão de colocar as fotorreceptores no sentido contrário ao da luz, e suas ligações serem posicionadas na direção da luz! Porém, é exatamente o que ocorre em todas as retinas dos vertebrados. Cada fotorreceptor é, de fato, embutido de trás para frente, com seus feixes nervosos ligados ao lado das células mais próximo da luz. Os feixes nervosos tem de atravessar a superfície da retina até um ponto onde ele “mergulha” dentro de uma abertura na retina (o chamado “ponto cego”) afim de chegarem ao nervo ótico. Isso significa que a luz, ao invés de ter garantida passagem livre direto até as fotorreceptores  tem de passar por uma floresta de feixes conectados, presumivelmente sofrendo ao menos alguma atenuação e distorção (na verdade, provavelmente não muita, de qualquer jeito, é o tipo de coisa que ofenderia qualquer engenheiro em perfeito juízo). Eu não sei a exata explicação para este estranho fato. O período relevante de sua evolução jaz no passado longínquo.’ 1

 

Primeiro, vamos revisar alguns pontos sobre a anatomia ocular:

 

 

A luz entra no olho humano pela transparente córnea, a janela frontal ocular, que age como uma poderosa lente convexa. Após passa pela pupila (a abertura no diafragma da íris) a luz e posteriormente refratada pela cristalino. Uma imagem do ambiente externo é então focalizada na retina que transforma a luz em sinais nervosos e é a mais profunda (em relação ao centro do globo ocular) das três “túnicas” do segmentos posterior do olho. As outras duas são a altamente fibrosa esclerótica (o “branco dos olhos”) encontrada na parte mais externa continuando desde a córnea e a coroide  uma camada altamente pigmentada e irrigada que se encontra entre as outras duas.

 

A retina consiste de 10 camadas, das quais a mais externa é a escura camada do epitélio pigmentar da retina (RPE em inglês) que devido ao pigmento melanina, é opaca a luz. Suas células tem finas projeções capilares em sua superfície interna chamada microvilosidades que permeiam a região e recobrem as pontas dos fotorreceptores dos segmentos externos. Daí existir um potencial ponto de fissão entre o RPE e os fotorreceptores que se torna evidente quando a retina se separe do RPE, tipo durante o resultado de uma lesão, uma condição conhecida como deslocamento de retina. Cada receptor, seja um bastonete ou cone, consiste de um segmento interior e um exterior, o primeiro contendo organelas para a fabricação dos pigmentos fotossensíveis presente no último. A camada de cones e bastonetes e todas as 8 camadas internas constituem o que é conhecido como retina neurosensorial que é virtualmente transparente à luz. Por meio de inúmeras conexões nervosas complexas dentro da retina neurosensorial, impulsos elétricos gerados pela luz ao atingirem os fotorreceptores são processados e transmitidos a camada de fibras nervosas da retina, de onde seguem pelo nervo ótico até o cérebro.

 

Em muitas espécies que necessitam de visão em ambientes de baixíssima iluminação, uma camada de material cristalino reflexivo, o tapetum (tapete em latim) é incorporado ao RPE ou a coróide. Agindo como um espelho, o tapetum reflete a luz que passa entre os fotorreceptores  daí aumentando a quantidade de luz atingindo os receptores.

 

 

O epitélio pigmentar da retina

 

Fundamental para o entendimento da retina invertida é o papel crucial do RPE. Muitas de suas essenciais funções ainda não são bem conhecidas. Cada célula do RPE está em contato intimo com as pontas dos 20 ou mais segmentos fotorreceptores exteriores cujo número chega a 130 milhões. Sem o RPE os receptores e o resto da retina neurosensorial não podem funcionar plenamente e acabariam se atrofiando.

 

O segmento externo de um receptor consiste de uma pilha de discos contendo pigmentos fotossensíveis. Estes discos são constantemente formados no segmento interno de onde eles seguem sucessivamente dos segmentos externos em direção ao RPE que recicla seus componentes químicos pelo processo de fagocitose (Grego:φάγω (phagō) = comer).

 

O RPE armazena vitamina A, um precursor dos pigmentos fotossensíveis  e em seguida participa de suas regenerações. Existem quatro fotopigmentos que se desbotam sob exposição à luz: rodopsina (encontrada em bastonetes, para visão noturna) e mais três tipos um para cada tipo de cone (um cone para cada cor primária). Ele sintetiza glicosaminoglicanas para o interfotorreceptor matriz, ou seja, o material interno que separa os receptores.

 

Além de oxigênio, o RPE seletivamente transporta nutrientes da coroide para suprir as três camadas externas da retina e remove os produtos residuais metabólicos dos receptores para serem varridos para circulação coroidal. Por meio de de seletivo bombeamento de metabólitos e a presença de estreitas junções intercelulares, o RPE age como uma barreira, prevenindo o acesso de resíduos químicos maiores ou nocivos ao tecido retinal, com isso contribuindo com a constante manutenção de um ambiente retinal estável e otimizado.

 

O RPE possui complexos mecanismos para lidar com molécula tóxicas e radicais livres produzidos pela ação da luz. Enzimas especializadas superóxido dismutases, catalases e peroxidases estão presentes para catalizar a quebra de potencialmente danosas moléculas como superóxido e o peróxido de hidrogênio. Antioxidantes tipo o atocoferol (vitamina E) e ácido ascórbico (vitamina C) estão presentes para reduzir os danos da oxidação.

 

Nossos receptores continuamente sintetizam novos discos com seus respectivos pigmentos fotossensíveis  reciclando materiais dos discos usados que foram dantes digeridos pelo RPE. Isto levanta a questão: ‘Porque existe esse tão complicado processo?’ A resposta pode estar no fato desse processo ser um exemplo de renovação biológica, pelo qual tecidos expostos a substâncias tóxicas, radiação, trauma físico, etc, podem sobreviver. Sem auto-renovação, tecidos como a pele, o revestimento do intestino, células sanguíneas e todo o resto iriam rapidamente acumular defeitos fatais. Do mesmo jeito, pela continua substituição dos discos os fotorreceptores superam o incessante processo de desintegração acelerado por agentes tóxicos, em particular, por luzes de comprimento de ondas curtas.

 

O dissipador térmico coroidal

 

 

Têm sido observado que o dano aos receptores de modelos experimentais está fortemente relacionado com a temperatura, e outros estudos confirmam que calor potencializa lesões fotoquímicas. Qualquer sistema projetado para resistir ao último deve também proteger contra o primeiro. Em 1980, um artigo foi publicado explicando pela primeira vez algo já conhecido sobre a coroide  2 Isto é, sua altíssima taxa de fluxo sanguíneo que excede em léguas a demanda nutricional da retina, apesar desta ser altamente ativa, metabolicamente, como já indicado.

 

Os vasos capilares coroidais (coriocapilares) formam um rico emaranhado na parte externa do RPE, predominantemente em sua área central, e separado deste apenas por uma fina membrana (membrana de Bruch). A absorção de luz excessiva pelo RPE produz calor na parte externa da retina que deve ser dissipado, afim de evitar danos pelo excesso de aquecimento ao delicado e complexo aparato biológico, e também a suas circunvizinhanças.

 

Os autores deste estudo contundentemente demonstram uma função essencial da coróide seu fluxo torrencial sanguíneo e sua proximidade ao RPE, serve para funcionar como dissipador de calor e resfriador. Ainda mais fascinante são os resultados de estudos posteriores pelos mesmos autores indicando que existem reflexos nervosos centrais (pelo cérebro) mediados pela luz que regulam o fluxo sanguíneo coroidal, aumentando o fluxo sanguíneo conforme a iluminação aumenta. Ambos RPE e coróide tem de estar localizados na parte externa da retina neurosensorial; disso podemos concluir que existem sólidas razões para a configuração invertida da retina de humanos e outros vertebrados.

 

A fóvea

 

Embora a retina neurosensorial seja virtualmente transparente excetuando-se em seus finíssimos vasos sanguíneos, existe um refinamento adicional de sua estrutura em sua região central chamada de mácula lútea. A retina e o córtex cerebral ocipital (chamado de córtex visual), para o qual a retina transmite informações visuais, é tão organizado que o VA é máximo no eixo visual. O eixo visual passa pela fovéola que forma o “piso” de uma fenda circular com uma parede declinada, chamado de fóvea (do latim= fenda, fossa) no centro da mácula. Longe da fóvea o VA diminui progressivamente em direção a periferia da retina. Daí os fotorreceptores de cor- os cones que detectam vermelho, verde e possivelmente azul- tem a maior densidade de 150.000 por mm² na fovéola  que mede apenas 300-330 µm de extensão.

 

O pigmento xantofila

 

O sistema ótico do olho humano é projetado de tal maneira que a luz ambiente tende a atingir com toda intensidade a área macular da retina, e com muito menos intensidade a periferia desta. É significante que não apenas a quantidade de melanina é mais abundante na região macular devido a suas células RPE serem maiores e mais numerosas por milimetro quadrado do que em qualquer outro lugar, mas também no centro da retina encontra-se o pigmento xantofila (Grego: ξάνθος- xanthos, amarelo). Nesta região, xantofila permeia todas as camadas da retina neurosensorial entre suas duas membranas e é concentrada nas células retinais, ambos os neurônios e células dos tecido que os sustenta. Atenção tem sido dada recentemente a presença de uma coleção de tecidos celulares de suporte chamada de tecidos de Muller que se encontram na superfície da fóvea e formam um cone cuja ponta pluga na depressão foveolar.

Xantofila é um carotenoide quimicamente ligado a vitamina A, cujo ápice do espectro de absorção chega a 460 nm e varia de 480 nm a 390 nm. Ela ajuda a proteger a retina neurosensorial ao absorver maior parte das ondas mais curtas da luz visível, ou seja, o espectro azul e violeta, potencialmente mais danosos.

 

 

O ponto cego

 

Devido a disposição invertida da retina, os axônios (fibras nervosas) que transmitem dados ao cérebro passam por baixo da superfície interna da retina e convergem em um pequeno ponto que é a “cabeça” do nervo ótico, daí, saindo para o cérebro. A cabeça do nervo ótico não possui receptores de luz, sendo portanto cega, causando um pequeno ponto cego no campo de visão. Sem surpresa, evolucionistas criticaram isso. Williams coloca o seguinte:

 

‘Nosso ponto cego da retina raramente causa alguma dificuldade, mas raramente não quer dizer nunca. Quando por um momento cubro um olho para repelir um inseto, um evento importante pode estar focalizado no ponto cego do outro.’ 3

 

Além disso, o problema tem de ser visto em perspectiva: o ponto cego é encontra-se a 15° do centro do eixo visual (a 3.7 mm da fovéola  e é minúsculo em relação ao campo de visão do olho, ocupando menos de 0.25% deste. Como mencionado acima, quanto mais longe da fovéola um ponto na retina está, menor será seu VA e sua sensibilidade. A retina ao redor da cabeça do nervo ótico, possui um VA apenas 15% igual ao da fovéola  Podemos inferir com segurança que o risco em teoria, previsto por Williams decorrente do ponto cego em uma pessoa de um olho só, é insignificante; e, em concordância com isso, é considerado seguro para uma pessoa de um olho só dirigir um carro privado, ou seja, para fins não profissionais.’

 

Como os dois campos visuais se sobrepõem em grande parte, o ponto cego de um olho é coberto pelo campo visual do outro. É verdade que a oclusão ou perda de um dos olhos é uma desvantagem, mas isso não é por causa do ponto cego do olho que notamos pelas razões expostas acima.

 

Olhos dos invertebrados

 

Algumas alegações de que a retina não-invertida de cefalópodes, tais como lulas e polvos, são mais eficientes do que a retina invertida encontrada em vertebrados. Mas isso pressupõe que a retina invertida é ineficiente, em primeiro lugar, e já vimos que não é o caso.

 

Além disso, eles nunca demonstraram que os cefalópodes realmente enxergam melhor. Pelo contrário, seus olhos apenas ‘se aproximam a alguns dos olhos de vertebrados inferiores em termos de eficiência’ e são provavelmente cegos de cores (só enxergam preto e branco). Além disso, a retina de cefalópodes, além de ser “convertida”, é muito mais simples do que a retina “invertida” de vertebrados; como Budelmann afirma, ‘A estrutura da retina [de cefalópodes] é muito mais simples do que do olho dos vertebrados, com apenas dois componentes neurais, células receptoras e fibras eferentes.’ É uma estrutura ondulante com ‘longas células fotorreceptoras cilíndricas com omatídeos consistindo de microvilosidades’, portanto os olhos de moluscos tem sido descrito como um “olho composto com lentes simples”. Finalmente, eles vivem em regiões com muito menos intensidade de luz do que a maioria dos vertebrados, o que contribui para demonstrar que olhos de cefalópodes não precisam ser tão complexos como é costumeiramente afirmado.

Apesar dos esforços de proponentes da evolução, a retina invertida não é evidência de “bad design”; pelo contrário, mesmo sua “fiação ao contrário” mostrar ser um sinal de criação planejada, para atender as demandas de cada ser vivo, de acordo com seu respectivo habitat.

 

(Do artigo: Is our ‘inverted’ retina really ‘bad design’?-Creation Ministries)

 

 

Referências

  •   Duke-Elder, S., System of Ophthalmology, Henry Kimpton, London, vol. 1, p. 147, 1958. 

  • Dawkins, R., The Blind Watchmaker: Why the evidence of evolution reveals a universe without design. W.W. Norton and Company, New York, p. 93, 1986. 

  • Duke-Elder, Ref. 1, pp. 608–609. 

  • Hogan, M.J., Alvarado, J.A., Weddell, J.E., The Retina. In Histology of the Human Eye, pp. 393–522, 1971. W.B. Saunders, Philadelphia. As cited in Tasman W., Jaeger E.A. (eds), Foundations of Clinical Ophthalmology, Lippincott–Raven, New York, vol. 1, ch. 21, 1998. 

  • Zinn, K.M., Benjamin-Henkind, J., Anatomy of the human retinal pigment epithelium, 1979. In Zinn, K.M., Marmot, M.F. (eds.), The Retinal Pigment Epithelium, Harvard University Press, Cambridge, MA, pp. 3–31. As cited in Tasman W., Jaeger E.A. (eds.), 

  • The photoreceptors are of two types: the rods which number about 125 million and the cones about 6.5 million. 

  • LaVail, M.M., Outer segment disc shedding and phagocytosis in the outer retina, Trans. Ophthalmol. Soc. UK 103:397, 1983.

  • Steinberg, R.H., Research update: report from a workshop on cell biology of retinal detachment,Exp. Eye Res. 43:696–706, 1986. 

  • Törnquist, P., Alm, A., Bill, A., Permeability of ocular vessels and transport across the blood-retinal barrier, Eye 4: 303–309, 1990. 

  • Grierson, I., Hiscott, P., Hogg, P., Robey, H., Mazure, A., Larkin, G., Development, repair and regeneration of the retinal pigment epithelium, Eye 8: 255–262, 1994. 

  • Kennon Guerry, R., Ham, W.T., Mueller, H.A. Light toxicity in the posterior segment, 1998. In Tasman W., Jaeger E.A. (eds.), Clinical Ophthalmology, Lippincott-Raven, New York, vol. 3, ch. 37. 

  • Young, R.W., The Bowman Lecture: Biological renewal: Applications to the eye, Trans. Ophthalmol. Soc. UK 102:42–67, 1982. 

  • Geeraets, W.J., Williams, R.C., Chan, G., Ham, W.T., Guerry, D., Schmidt, F.H., The loss of light energy in retina and choroid, Arch. Ophthalmol. 64:158, 1960. As cited by Parver, L.M. et al.,

  • Photon energy (E) is inversely proportional to wavelength (λ): E = hc/λ, where h is Planck’s Constant and c is the speed of light in a vacuum. 

  • Spectroscopic terms like ‘singlet’, ‘doublet’, ‘triplet’ etc. refer to the number of possible orientations of the total electronic spin of the molecule in a magnetic field. The ground (lowest energy) state of the O2 molecule is a triplet state (3Σg–) with two unpaired electrons. But when excited by a photon, it moves into a higher energy (thus more reactive) singlet state (1Δg) with no unpaired electrons. 

  • Noell, W.K., Walker, V.S., Kang B.S. et al., Retinal damage by light in rats, Invest. Ophthalmol. 5:450, 1966.

  • Friedman, E., Kuwubara, T., The retinal pigment epithelium: IV. The damaging effects of radiant energy, Arch. Ophthalmol. 80:265–279, 1968. 

  • Parver, L.M., Auker, C., Carpenter, D.O., Choroidal blood flow as a heat dissipating mechanism in the macula, Am. J. Ophthalmol. 89:641–646, 1980. 

  • Parver, L.M., Auker, C., Carpenter, D.O., Choroidal blood flow: III. Reflexive control in the human, Arch. Ophthalmol. 101:1604, 1983.

  • Parver, L.M., Temperature modulating action of choroidal blood flow, Eye 5:181, 1991. 

  • Wieland, C.Seeing back to front: Are evolutionists right when they say our eyes are wired the wrong way? Creation 18(2):38–40, 1996. 

  • Anon., An eye for creation: an interview with eye disease researcher Dr G. Marshall, University of Glasgow, Scotland , Creation 18(4):19–21, 1996. 

  • The cerebral cortex is the grey cellular mantle (1–4 mm thick) forming the entire surface of the cerebral hemisphere of mammals. In man and the primates, part of the occipital cortex (at the posterior pole of each hemisphere) is specialised to receive signals from the two retinas and not until this level is reached by retinal signals is there conscious visual perception. The central 1.5 mm of the retina (the macula) has disproportionate representation in the visual cortex, amounting to about half of its area. 

  • The cones for blue are much less numerous than those for red and for green and it is now thought that they may not be present in the foveola. 

  • Osterberg, G., Topography of the layer of rods and cones in the human retina, Acta Ophthalmol. (suppl.) 6:1, 1935. As cited in Tasman W., Jaeger E.A. (eds), Ref. 4, vol. 1, ch. 21.

  • The foveola subtends an angle of about 20 minutes of arc at the nodal point of the eye while the normal resolving power of the eye or the angle subtended by the minimum perceivable separation of two points is 1 minute of arc. 

  • Visual signals arising in the receptors are relayed in the retina first via the bipolar cells in the inner nuclear layer and then via the ganglion cells whose axons or nerve fibres form the nerve fibre layer of the retina. 

  • Curio, C.A., Allen, K.A., Topography of ganglion cells in human retina, J. Comp. Neurol. 300:5, 1990. As cited in Tasman W., Jaeger E.A. (eds), Ref. 4, vol. 1, ch. 19. 

  • Schein, S.J., Anatomy of macaque fovea and spatial densities of neurons in foveal representation, J. Comp. Neurol. 269:479, 1988. Cited in: Tasman W., Jaeger E.A. (eds), ref. 4, vol. 1, ch. 19. 

  • Streeten, B.W., Development of the human retinal pigment epithelium and the posterior segment, Arch. Ophthalmol. 81:383–394, 1969. 

  • Identifying the precise location of xanthophyll, i.e. the layers and structures in which it is present within the neurosensory retina has proved difficult for investigators but there is a consensus for what is given here.

  • Gass, J.D.M., Müller Cell Cone, an Overlooked Part of the Anatomy of the Fovea Centralis, Arch Ophthalmol. 117:821–823, 1999. 

  • This graph is based on information from various sources as indicated by the references. Some absorption curves for melanin show an apparent fall-off at the short wavelength end of the light spectrum but this is caused by reduced transmission of short wavelength radiation by the ocular media (the cornea and more so the crystalline lens), rather than by a decrease in absorption by melanin granules. 

  • Sabates, F.N., Applied laser optics: Techniques for retinal laser surgery, 1997. In Tasman W., Jaeger E.A. (eds), 1997. Clinical Ophthalmology, Lippincott-Raven, New York, vol. 1, ch. 69A.

  • Nussbaum, J.J., Pruett, R.C., Delori, F.C., Historic perspectives. Macular yellow pigment. The first 200 years, Retina 1:296–310, 1981. 

  • Duke-Elder, S. (ed), Ref. 1, vol. 2, p. 264, 1961.

  • The degree of scattering is inversely proportional to the fourth power of the wavelength. 

  • Ham, W.T. Jr., Mueller, H.A., Ruffolo, J.J. Jr. et al., Action spectrum for retinal injury from near-ultraviolet radiation in the aphakic monkey, Am. J. Ophthalmol.93:299, 1982. [The term aphakia means absence of the lens in the eye. The eyes of monkeys were subjected to the experiments after their lenses had been removed.] 

  • Boettner, E.A., Wolter, J.R., Transmission of the ocular media, Invest. Ophthalmol. Vis. Sci 1:776, 1962. Cited in: Tasman W., Jaeger E.A. (eds), Ref. 11, vol. 5, ch. 55. 

  • The eyes are further shielded from excessive exposure to light and UVR by anatomical features: the normal horizontal orientation of the eyes when in the upright posture, the eyebrows (particularly for those with deep-set eyes), the nose and the cheeks. But any natural defence system can be overwhelmed and so it is sensible when necessary (just as it is to wear extra clothing in cold weather) to wear or use extra protection against UVR and blue light; all the more is this so with the depletion of our ozone layer. 

  • Williams, G.C., Natural Selection: Domains, Levels and Challenges, Oxford University Press, Oxford, pp. 72–73, 1992. 

  • Traquair, H.M., An Introduction to Clinical Perimetry, The C V Mosby Co., St Louis, 1938.

  • Wertheim, Z., Psychol. Physiol. Sinnes. 7:172, 1894. Cited in: Duke-Elder, S. (ed.), Ref. 1, vol. 4, p. 611, 1968. 

  • The reduction of overall visual field with the loss or occlusion of one eye amounts to 20–25% with the seeing eye looking straight ahead, mainly on account of the nose. The field of each eye is normally restricted by the facial contours mentioned in endnote 40. The field loss caused by the nose is largely recovered if the subject turns the head a little towards the blind side; this is often done unconsciously by a one-eyed person when looking intently. Return to text.

  • Diamond, J., Voyage of the Overloaded Ark, Discover, June, pp. 82–92, 1985.

  • Mollusks, Encyclopædia Britannica 24:296-322, 15th ed., 1992; quote on p. 321.

  • Hanlon, R.T., and Messenger, J.B., Cephalopod Behaviour, Cambridge University Press, Cambridge, New York, p. 19, 1996.

  • Budelmann, B.U., Cephalopod sense organs, nerves and brain, 1994. In Pörtner, H.O., O’Dor, R.J. and Macmillan, D.L., ed., Physiology of cephalopod molluscs: lifestyle and performance adaptations, Gordon and Breach, Basel, Switzerland, p. 15, 1994.

  • Sensory Reception, Encyclopædia Britannica 27:114–221, 15th ed., 1992; quote on p. 147.

Our inverted retina: Not a bad design

Evolutionists frequently maintain that the vertebrate retina exhibits a feature which indicates that it was not designed because its organisation appears to be less than ideal. They refer to the fact that for light to reach the photoreceptors it has to pass through the bulk of the retina’s neural apparatus, and presume that consequent degradation of the image formed at the level of the photoreceptors occurs. In biological terms this arrangement of the retina is said to be inverted because the visual cells are oriented so that their sensory ends are directed away from incident light. It is typical of vertebrates but rare among invertebrates, being seen in a few molluscs and arachnids.

 

 

 

 

 

 

As usual, evolutionists like to point this out as an evidence of “bad design”, thus, being supposedly more explainable under the light of natural, unguided view. Dawkins, while admitting that light traversing the inverted retina is not disturbed significantly during its passage to the photoreceptors, writes as follows :

‘Any engineer would naturally assume that the photocells would point towards the light, with their wires leading backwards towards the brain. He would laugh at any suggestion that the photocells might point away, from the light, with their wires departing on the side nearest the light. Yet this is exactly what happens in all vertebrate retinas. Each photocell is, in effect, wired in backwards, with its wire sticking out on the side nearest the light. The wire has to travel over the surface of the retina to a point where it dives through a hole in the retina (the so-called ‘blind spot’) to join the optic nerve. This means that the light, instead of being granted an unrestricted passage to the photocells, has to pass through a forest of connecting wires, presumably suffering at least some attenuation and distortion (actually, probably not much but, still, it is the principle of the thing that would offend any tidy-minded engineer). I don’t know the exact explanation for this strange state of affairs. The relevant period of evolution is so long ago.’ 1

First, we must review some things about ocular anatomy:

 

Figure 2Light enters the human eye via the transparent cornea, the eye’s front window, which acts as a powerful convex lens. After passing through the pupil (the aperture in the iris diaphragm) light is further refracted by the crystalline lens. An image of the external environment is thus focused on the retina which transduces light into neural signals and is the innermost (relative to the geometric centre of the eyeball) of the three tunics of the eye’s posterior segment. The other two tunics of the eye’s posterior segment are the white tough fibrous sclera which is outermost and continuous with the cornea anteriorly, and thechoroid, a pigmented and highly vascular layer which lies sandwiched between the retina and sclera.

The retina consists of ten layers, of which the outermost is the dark retinal pigment epithelium (RPE) which because of its melanin pigment is opaque to light. The RPE cells have fine hair-like projections on their inner surface called microvilli which lie between and ensheath the tips of the photoreceptor outer segments. There is thus a potential plane of cleavage between the RPE and the photoreceptors which is manifested when the neurosensory retina becomes separated from the RPE, e.g. as a result of injury, a condition known as retinal detachment.

Each photoreceptor, whether rod or cone, consists of an inner and an outer segment, the former having organelles (intracellular apparatus) for manufacturing the visual pigment present in the latter. The rod and cone layer and all eight layers internal to it constitute (in distinction from the RPE) what is known as the neurosensory retina which is virtually transparent to light. By means of many complex nerve connections within the neurosensory retina, electrical impulses generated by light reaching the photoreceptors are processed and transmitted to the retina’s nerve fibre layer and thence pass up the optic nerve to the brain.

In many species for whom vision in very low levels of illumination is important, a layer of reflective crystalline material, the tapetum (Latin: carpet) is incorporated in the RPE or choroid.1 Acting as a mirror, the tapetum reflects light which has passed between the photoreceptors, so augmenting the light bombarding the photoreceptors. Hence the proverbial ‘cat’s eyes’ when caught by a beam of light in the dark.

The retinal pigment epithelium

Fundamental to understanding the inverted retina is the crucial role played by the RPE. Many of its important functions are now well known. Each RPE cell is in intimate contact with the tips of 20 or more photoreceptor outer segments which number over 130 million. Without the RPE the photoreceptors and the rest of the neurosensory retina cannot function normally and ultimately atrophy.

The outer segment of a photoreceptor consists of a stack of discs containing light-sensitive photopigment. These discs are being continually formed by the inner segment from where they move in succession outwards in the outer segment towards the RPE which phagocytoses (Greek: φάγω (phagō) = eat) them and recycles their chemical components.

The RPE stores vitamin A, a precursor of the photopigments, and thus participates in their regeneration. There are four photopigments which are all bleached on exposure to light: rhodopsin (found in the rods, for night vision) and one for each of the three different types of cones (one for each of the primary colours). It synthesises glycosaminoglycans for the interphotoreceptor matrix, i.e. the material lying between and separating the photoreceptors.

Besides oxygen, the RPE selectively transports nutrients from the choroid to supply the outer third of the retina and removes the waste products of photoreceptor metabolism to be cleared by the choroidal circulation. By selective pumping of metabolites and the presence of its tight intercellular junctions, the RPE acts as a barrier, called the blood-retinal barrier, preventing access of larger or harmful chemicals to retinal tissue, thereby contributing to the maintenance of a stable and optimal retinal environment.

The RPE has complex mechanisms for dealing with toxic molecules and free radicals produced by the action of light. Specific enzymes such as the superoxide dismutases, catalases, and peroxidases are present to catalyse the breakdown of potentially harmful molecules such as superoxide and hydrogen peroxide. Antioxidants such as a-tocopherol (vitamin E) and ascorbic acid (vitamin C) are available to reduce oxidative damage.

Our photoreceptors thus continually synthesise new outer segment discs with their specific photopigments, recycling materials from used discs digested by the RPE. This prompts the question, ‘Why have such a complicated process?’ The answer must be that it is an example of biological renewal, by means of which tissues exposed to damaging chemicals, radiation, mechanical trauma, etc., are able to survive. Without self renewal, tissues such as the skin, the lining of the gut, blood cells etc would quickly accumulate fatal defects. In the same way, by the continual replacing of their discs the photoreceptors counter the relentless process of disintegration accelerated by toxic agents, particularly short wavelength light.

 

The choroidal heat sink

 

It has been observed that the damage to photoreceptors in an experimental model is strongly related to temperature, and other studies have confirmed that heat exacerbates photochemical injury. Any system designed to protect against the latter should also protect against the former. In 1980, a paper was published which explained for the first time something already known about the choroid.2 That is, its very high rate of blood flow which far exceeds the nutritional needs of the retina, despite the latter being highly active metabolically, as indicated.

The choroidal capillaries (the choriocapillaris) form a rich plexus lying immediately external to the RPE, predominantly its central area, and separated from it by only a very thin membrane (Bruch’s). The absorption of excess light by the RPE produces heat in the outer retina which has to be dissipated if thermal damage to the delicate and complex biological machinery, its own and that of its neighbourhood, is to be avoided.

The authors of this study cogently argue that an important function of the choroid with its torrential blood flow (in local terms) and its close proximity to the RPE, is to act as a heat sink and cooling device. Still more fascinating are the results of further studies by the same workers indicating that there are central (via the brain), light-mediated nervous reflexes regulating choroidal blood flow, increasing the blood flow with increased illumination. Both RPE and choroid are essential for vision, but they are opaque, so it follows that for light to reach the photoreceptors, both RPE and choroid have to be located external to the neurosensory retina; hence we can conclude that there are sound reasons for the inverted configuration of the human and vertebrate retina.

 

The foveola

Although the neurosensory retina is virtually transparent apart from the blood in its very slender blood vessels, there is an additional refinement of its structure in its central region called the macula. The retina and the occipital cerebral cortex (called the visual cortex) of the brain, to which the former transmits visual information, are so organised that the VA is maximal in the visual axis. The visual axis passes through the foveola which forms the floor of a circular pit with a sloping wall, the fovea (Latin: pit) at the centre of the macula. Away from the fovea the VA diminishes progressively towards the periphery of the retina. Thus the colour photoreceptors—the cones for red, green and possibly also blue—have their greatest density of 150,000 per square mm at the foveola, which measures only 300–330 µm across.

 

Xanthophyll pigment

The optical system of the human eye is such that ambient light tends to fall with peak intensity on the macular area of the retina with much less on the retinal periphery. It must be significant therefore that not only is melanin more abundant in the macular region because its RPE cells are taller and more numerous per unit area than elsewhere30 but there is also in the retina’s central area the yellow pigment xanthophyll (Greek: ξάνθος xanthos, yellow). In this region of the retina, xanthophyll permeates all layers of the neurosensory retina between its two limiting membranes and is concentrated in the retinal cells, both the neurons and the supporting tissue cells. Recently attention has been drawn to the presence of a collection of retinal supporting tissue cells (called Müller cells after the person who first described them) over the internal surface of the fovea and forming a cone whose apex plugs the foveolar depression.

Retinal xanthophyll is a carotenoid, chemically related to vitamin A, whose absorption spectrum peaks at about 460 nm and ranges from 480 nm down to 390 nm It helps to protect the neurosensory retina by absorbing much of the potentially damaging shorter wavelength visible light, i.e. blue and violet, which is more scattered by small molecules and structures.

 

The blind spot

Because of the retina’s inverted arrangement, the axons (nerve fibres) transmitting data to the brain pass under cover of the retina’s inner surface to converge to a small area which is the optic nerve head, where they all exit the eye together as the optic nerve. The optic nerve head has no photoreceptors and so is blind, thereby producing a small blind spot in the visual field. No surprise, evolutionists criticized that. As Williams puts it:

‘Our retinal blind spots rarely cause any difficulty, but rarely is not the same as never. As I momentarily cover one eye to ward off an insect, an important event might be focused on the blind spot of the other.’ 3
Notwithstanding, this issue has to be viewed in perspective: the blind spot is centred at 15° away from the visual axis (3.7 mm from the foveola) and is very small in relation the visual field of an eye, occupying less than 0.25%. As mentioned above, the further away a point in the retina is from the foveola, the less will be its VA and its sensitivity. The retina surrounding the optic nerve head, in the light-adapted state, has a VA of only about 15% of that at the foveola. We can safely infer that the theoretical risk referred to by Williams arising from the blind spot in a one-eyed person, is negligible; and, in keeping with this, it is considered safe for a one-eyed person to drive a private motor car, i.e. for non-vocational purposes.’ 

Because the two visual fields overlap to a large degree, the blind spot of one eye is covered by the other eye’s visual field. It is true that occlusion or loss of one eye is a handicap, but this is not because of the blind spot of the seeing eye for the reasons given above.

 

Invertebrated eyes

Some claims that the verted retinae of cephalopods, such as squids and octopuses, are more efficient than the inverted retinae found in vertebrates. But this presupposes that the inverted retina is inefficient in the first place, and we’ve seen that isn’t the case. Also, they have never shown that cephalopods actually see better. On the contrary, their eyes merely ‘approach some of the lower vertebrate eyes in efficiency’ and they are probably colour blind. Further, the cephalopod retina, besides being ‘verted’, is actually much simpler than the ‘inverted’ retina of vertebrates; as Budelmann states, ‘The structure of the [cephalopod] retina is much simpler than in the vertebrate eye, with only two neural components, the receptor cells and efferent fibres’.5 It is an undulating structure with ‘long cylindrical photoreceptor cells with rhabdomeres consisting of microvilli’, so that the cephalopod eye has been described as a ‘compound eye with a single lens’. Finally, they live in regions with much lower light intensity than most vertebrates, which contributes to show that cephalopods eyes don’t need to be so complex as it’s usually claimed.

Despite the efforts of evolution promoters, the inverted retina isn’t an evidence of bad design; all the way around, even its “backwards wired” design poses a clear sign of planned origin, as to suit the demands of each living being, in accordance to its environment.

(From the article:  Is our ‘inverted’ retina really ‘bad design’?-Creation Ministries)

 

God bless you!

 

References

 

1 Dawkins, R., The Blind Watchmaker: Why the evidence of evolution reveals a universe without design. W.W. Norton and Company, New York, p. 93, 1986

2 Duke-Elder, S., System of Ophthalmology, Henry Kimpton, London, vol. 1, p. 147, 1958.

3 Parver, L.M., Auker, C., Carpenter, D.O., Choroidal blood flow as a heat dissipating mechanism in the macula, Am. J. Ophthalmol. 89:641–646, 1980.

4 Williams, G.C., Natural Selection: Domains, Levels and Challenges, Oxford University Press, Oxford, pp. 72–73, 1992.

5 Budelmann, B.U., Cephalopod sense organs, nerves and brain, 1994. In Pörtner, H.O., O’Dor, R.J. and Macmillan, D.L., ed., Physiology of cephalopod molluscs: lifestyle and performance adaptations, Gordon and Breach, Basel, Switzerland, p. 15, 1994.

Human–chimp DNA similarity re-evaluated

A review of the common claim that the human and chimpanzee (chimp) genomes are nearly identical was found to be highly questionable solely by an analysis of the methodology and data outlined in an assortment of key research publications. Reported high DNA sequence similarity estimates are primarily based on prescreened biological samples and/or data. Data too dissimilar to be conveniently aligned was typically omitted, masked and/or not reported. Furthermore, gap data from final alignments was also often discarded, further inflating final similarity estimates. It is these highly selective data-omission processes, driven by Darwinian dogma, that produce the commonly touted 98% similarity figure for human–chimp DNA comparisons. Based on the analysis of data provided in various publications, including the often cited 2005 chimpanzee genome report, it is safe to conclude that human–chimp genome similarity is not more than ~87% identical, and possibly not higher than 81%.

 

 


A common claim is that the DNA of chimpanzees (Pan troglodytes) and humans (Homo sapiens) are about 98% similar. This oversimplified and often-touted estimate can actually involve two completely separate concepts. 1) Gene content (the comparative counts of similar types of coding sequences present or absent between different species) and 2) similarities between the actual base pairs of DNA sequences in alignments. For the most part, the modern similarity paradigm refers to DNA sequence alignment research. Biological sequence data often goes through several levels of prescreening, filtering and selection before being summarized and discussed.

One of the major problems with overall research in the field of comparative genetics, as we will show, is that in most studies there is a great deal of preselection applied to the available biological samples and data before the final analysis is undertaken. Only the most promising data from a larger pool is typically extracted for a final analysis.

 

Early human–chimp studies with reassociation kinetics

The initial estimates of high human-chimp DNA similarity came from a field of study called reassociation kinetics. These initial reports fueled early claims by such popular evolutionary luminaries as Oxford Professor Richard Dawkins, who stated “Chimpanzees and we share more than 99 per cent of our genes.” At the time, this statement was presumptuous, because gene numbers for humans and chimps were not known. The initial drafts of the human and chimp genomes were not announced until 2001 and 2005, respectively.

The supposed gene data Dawkins referred to in 1986 was an indirect estimate based on the reassociation kinetics of mixed human and chimp DNA, not clearly defined genes.1 In reassociation kinetics, heat and/or chemistry are used to separate double-stranded DNA into single strands. When the DNA is allowed to reassociate in a controlled manner, it can be fractionated using various protocols. The slower the reassociation, the more complex and gene-dense the DNA is thought to be. In general, three types of DNA can be recovered: high-copy (highly repetitive, gene poor), low-copy (moderately repetitive, low levels of genes), and single copy (gene-rich). For comparative studies, the single copy fraction of DNA is collected from two species, mixed together, disassociated and allowed to reassociate so that human and chimp DNA can recombine. The level of complementary base matching between strands can be indirectly measured by a variety of methods that indirectly measure rates/levels of reassociation.

The caveat is that only the single-copy fractions of the human and chimp genomes were utilized to obtain early estimates of similarity. Scientists focused on the single-copy fraction because of the high gene content. However, many genes are located in the other genome fractions and were thus left out of the analysis. Another problem is that virtually the entire genome is now known to be functional in some aspect and the non-coding regions have been shown to provide many critical control features and nucleotide templates.

 

Genomics research—affirming the myth

Subsequent research using sequenced DNA built upon the early high similarity dogma established by reassociation kinetics. In a companion to this paper, we discuss the possibility that an unspoken dogma-based ‘Gold Standard’ regarding the human–chimp similarity issue was established during the initial studies involving reassociation kinetics.

A review paper written by creationist Todd Wood on biological similarity between human and chimp highlighted and supposedly confirmed evolutionary similarity claims, yet ignored the important bioinformatic issues surrounding widespread data omission and selective analyses. Wood’s review did little to support creationist claims that humans were uniquely created in the image of God rather than being a few DNA base pairs from a chimp. Therefore, our focus on DNA sequence similarity will address the same publications listed in Wood’s review in addition to several more recent papers.

Reference

Total genomic bases analyzed

Aligned bases

Reported DNA identity

Actual DNA identity*

Britten, 2002

846,016

779,132

95.2%

~ 87%

Ebersberger et al., 2002

3,000,286

1,944,162

98.8%

< 65%

Liu et al., 2003

10,600,000 (total for human, chimp, baboon, and marmoset)

4,968,069 (human–chimp)

98.9% no indels

?

Wildman et al., 2003

~90,000 (exons from 97 genes)

?

98.4–99.4%

?

Chimp. Chrom. 22 Consort.

32,799,845

?

98.5% excluding indels

80–85% including indels

Nielson et al., 2005

?

?

99.4% selected gene regions

?

Chimp. Seq. Consort. 2005

Whole genome (5X redundant coverage)

2.4 Gb

95.8%

81%**

 

* Based on the amount of omitted DNA sequence in the alignments
** Compared to data from The International Human Genome Sequencing Consortium (2004)—((.9577 x 2.4 Gb) / 2.85 Gb) x 100
? Cannot calculate actual percent identity because data was not provided.

Roy Britten, one of the early pioneers in DNA reassociation kinetics, compared the genomic sequence from five chimp large-insert DNA clones (Bacterial Artificial Chromosomes, or BACs) to human genomic sequence using an atypical fortran-based computer program. These five chimp BAC sequences were chosen because they were the only ones then available.Researchers typically choose initial seed BACs for genome sequencing because of their single-copy DNA content, which makes them easier to assemble and compare to other species. The total length of the DNA sequence for all 5 BACs was 846,016 bases. However, only 92% of this was alignable to human DNA, thus the final statistics reported on only 779,132 bases. To his credit, Britten included the alignment data on insertions and deletions (indels) and reported a human–chimp similarity of ~95%. However, a more realistic figure would include the complete high-quality sequence of all five BACs, which is just as legitimate as the indels within the alignments; giving a final DNA similarity of 87%

 

Figure 1. Illustration showing the caveats of a hypothetical pairwise alignment between homologous sequences from two different species Figure 1.

Another notable study published by Ebersberger et al. the same year as Britten’s paper utilized chimp genome sequence obtained from randomly sheared, size-selected fragments in the 300 to 600 base range.These DNA sequences were aligned to an early version of the human genome assembly using the BLAT (Blast-Like Alignment Tool) algorithm. Researchers selected two-thirds of the total sequence for more detailed analyses. One-third of the chimp sequence would not align to the human genome and was discarded. The methods section in the paper19 describes how the subset of prescreened data was further filtered to obtain only the very best alignments. The resulting data was then subjected to a variety of comparative analyses that, for all practical purposes, are completely meaningless given the extremely high level of selection, data masking, and filtering applied. Not surprisingly, they report only a 1.24% difference in only highly similar aligned areas between human and chimp. A more realistic sequence similarity  is not more than 65% .

Shortly after these initial human–chimp comparison papers, a disturbing trend quickly emerged. This trend involved only reporting final alignment results and omitting the specific details of how such data was filtered, masked and selected. Key data to allow critical readers of human–chimp similarity papers to calculate a more accurate overall similarity began to be consistently omitted. For example, Liu et al. reported on the alignment of human genomic sequence with chimp, baboon, and marmoset. Important information concerning the starting set of sequences and specific data for the alignments was omitted. They state only that they used a total amount of 10.6 Mb of sequence for all species combined. Their similarity estimate on the final alignment, omitting indels and non-aligned areas, was 98.9%. Including indels, we derived a value of 95.6% for the alignments, similar to Britten’s research. Important data outside the aligned areas was impossible to evaluate because of the omitted sequence data.

Another disturbing trend is that only highly conserved protein-coding sequence (exons) are often utilized to report genome-wide similarity. We now know that non protein-coding sequences, which comprise greater than 95% of the genome, are critical to all aspects of genetics and genome function. Typical of the trend to only align exonic sequences, Wildman, et al. reported on a study that compared only human and chimp protein coding regions of 97 exon fragments for a total of 90,000 bases.

In 2004, Watanabe et al. used a variety of BAC libraries to select clones for DNA sequencing representing chimp chromosome 22. The sequence was then compared to its similar human homolog. The caveat is that the individual chimp BAC clones were only selected if they each contained 6 to 10 human DNA markers. Unfortunately, critical overall DNA alignment statistics are not given in the paper or in the supplemental information. The authors state a nucleotide substitution rate of 1.44% in aligned areas, but do not give similarity estimates to include indels. While indels are omitted from the alignment similarity, the authors indicate that there were 82,000 of them and provide a histogram that graphically shows the size distribution based on binned data groupings. Oddly, no data for average indel size or total indel length was provided. Likewise, the number of sequence gaps were given, but nothing about cummulative gap size.  Based on an estimate using the limited graphical data provided regarding base substitutions and indels, an estimate of about 80 to 85% overall similarity can be inferred.

One of the most ambiguous of all human–chimp studies was published by Nielson et al. In keeping with the established obfuscational trend, only highly conserved exons were used and no data were given to allow one to calculate any type of real overall similarity. Of the total starting number of gene sequences in the analysis (20,361) the researchers decided to throw out 33% (6,630) in an ambiguously stated “very conservative quality control”. In other words, one third of the initial chimp data did not align to human, so it got tossed out. In fact, no hard data was actually given.

 

Chimpanzee rough draft genome assembly data—81% similarity?

 

The major milestone publication regarding human–chimp genome comparisons was the 2005 Nature paper from the International Chimpanzee Genome Sequencing Consortium.4 Unfortunately, this paper followed the previously established trend where most of the comparative data was given in a highly selective and obfuscated format and detailed information about the alignments was absent. The majority of the paper was primarily concerned with a variety of hypothetical evolutionary analyses for various divergence rates and selective forces. Hence, the critical issue of overall similarity was carefully avoided.

However, based on the numbers given in the chimp genome paper, one can determine a rough overall genome similarity between humans and chimp by including published concurrent information from the human genome project. In regards to the overall alignment, the authors state, “Best reciprocal nucleotide-level alignments of the chimpanzee and human genomes cover ~2.4 gigabases (Gb) of high-quality sequence”. At this time, the human euchromatic assembly was estimated to be 99% complete at 2.85 Gb and had an error rate of 1 in 100,000 bases. The chimp genome authors state, “The indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions.”

In summary, only 2.3 Gb of chimp sequence aligned onto the highly accurate and complete human genome (2.85 Gb) an operation that included the masking of low complexity sequences. For the chimp sequence that aligned, the data for substitutions and indels indicates 95.8% similarity, a biased figure which excludes the masked regions. Using these numbers, an overall estimate of chimp compared to human DNA produces a conservative estimate of genome-wide similarity at 80.6%.

 

The paradigm starts to crumble

 

A study by Ebersberger et al., in which a large pool of human, chimp, orangutan, rhesus and gorilla genomic sequences was used in constructing phylogenies (multiple alignments analyzed in evolutionary tree format). The original pool of DNA sequences actually went through several levels of selection to preanalyze, trim and filter them for optimal alignment. First, a set of 30,112 sequences were selected that shared homology (overlapping similarity) between the five species. These sequences were aligned and only those which produced ≥ 300 base alignments were retained for another series of alignments and only the sequences that produced superior statistical probabilities > 95% were used in the final analysis. This filtering process removed over 22% of already-known, pre-selected homologous sequence. Despite all of this data filtering designed to produce the most favourable evolutionary alignment and trees, the results did not show any clear path of ancestry for humans with chimps or any of the great apes. What emerged was a true mosaic of unique human and primate DNA sequences; discounting any clear path of common ancestry. Perhaps the best summary of the research can be found in the author’s own words.

“For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee.

“Thus, in two-thirds of the cases a genealogy results in which humans and chimpanzees are not each other’s closest genetic relatives. The corresponding genealogies are incongruent with the species tree. In accordance with the experimental evidences, this implies that there is no such thing as a unique evolutionary history of the human genome. Rather, it resembles a patchwork of individual regions following their own genealogy.”

 

The Y-chromosome

One of the most intriguing studies is the Y-chromosome comparison between humans and chimps. In this study, the male-specific region (MSY), was compared between human and chimp. The result was 25,800,000 bases of highly accurate chimp Y-chromosome sequence distributed among eight contiguous segments. When compared to the human Y-chromosome, the differences were enormous. The authors state, “About half of the chimpanzee ampliconic sequence has no homologous, alignable counterpart in the human MSY, and vice versa.”

The ampliconic sequence contains ornate repeat units (called palindromes) that read the same forwards as they do backwards. Dispersed within these palindromes are families of genes that are expressed primarily in the male testes. Not only did 50% of this type of sequence fail to align between human and chimp in the Y-chromosome, humans had over twice as many total genes (60 in humans vs 25 in chimp). There were also three complete categories of genes (gene families) found in humans that were not even present in chimps. Related to this large difference in gene content, the authors note, “Despite the elaborate structure of the chimpanzee MSY, its gene repertoire is considerably smaller and simpler than that of the human MSY,” and “the chimpanzee MSY contains only two-thirds as many distinct genes or gene families as the human MSY, and only half as many protein-coding transcription units.”

A comparison of the so-called X-degenerate gene regions between humans and chimps also showed distinct organizational and locational differences in addition to differences in gene content. In fact, humans have three types (classes) of X-degenerate genes that are not even present in chimps.

Besides the large differences in gene content between human and chimp MSY regions, the overall structural differences were enormous. Take note of some of the additional comments from the authors:

“Moreover, the MSY sequences retained in both lineages have been extraordinarily subject to rearrangement: whole chromosome dot-plot comparison of chimpanzee and human MSYs shows marked differences in gross structure.

“The chimpanzee ampliconic regions are particularly massive (44% larger than in human) and architecturally ornate, with 19 palindromes (compared to eight in human) and elaborate mirroring of nucleotide sequences between the short and long arms of the chromosome, a feature not found in the human MSY.

“Of the 19 chimpanzee palindromes, only 7 are also found in the human MSY; the other 12 are chimpanzee-specific. Unlike the human MSY, nearly all of the chimpanzee MSY palindromes exist in multiple copies.”

The large differences in both structural arrangements of unique DNA features and gene content described in the Y-chromosome study, is particularly damaging to human-chimp DNA similarity mythos and the dogma of primate evolution. In fact, the authors shockingly note that given “ … 6 million years of separation, the difference in MSY gene content in chimpanzee and human is more comparable to the difference in autosomal gene content in chicken and human, at 310 million years of separation.”

A large study of genetic variation in the human genome showed that the Y-chromosome was exceptionally stable and had five times less genetic variation than the autosomes. This data makes perfect sense because the Y-chromosome has no similar homolog in the genome and undergoes very little recombination with the X-chromosome during meiosis. Given this lack of recombination and sequence diversity on the Y-chromosome, the primate evolution model encounters a serious problem, because the human and chimp Y-chromosomes should be considerably more similar to each other.

Some cases of high similarity may be due to contamination

Another factor to consider in the human-chimp similarity debate is that some cases of high sequence similarity may be due to contamination. Not only is the chimpanzee genome assembly still largely based on the human genomic framework, it also now appears that the wide-spread contamination of non-primate databases with human DNA is a serious problem and can run as high as 10% in some cases.Human contamination results from the process of cloning DNA fragments in the lab for sequencing where airborne human cells come from coughing, sneezing, and physical contact with contaminated fingers.

On a recent website at the Ensembl database (joint bioinformatics project between EMBL-EBI and the Wellcome Trust Sanger Institute), a webpage titled ‘Chimp Genebuild’ provides the following information as to one of the ways in which the human genome is used as a guide to assemble and annotate the chimp genome:

“Owing to the small number of proteins (many of which aligned in the same location) an additional layer of gene structures was added by projection of human genes. The high-quality annotation of the human genome and the high degree of similarity between the human and chimpanzee genomes enables us to identify genes in chimpanzee by transfer of human genes to the corresponding location in chimp.

“The protein-coding transcripts of the human gene structures are projected through the WGA [whole genome assembly] onto the chromosomes in the chimp genome. Small insertions/deletions that disrupt the reading-frame of the resultant transcripts are corrected for by inserting ‘frame-shift’ introns into the structure.”

 

From: Creation.com

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