Wednesday, April 15, 2009
Color Blind
On pages 94-98, Carroll discusses the evolution of color vision in humans and on pages 127-129 he discusses the subsequent loss of smell. Carroll states that "we no longer rely on our sense of smell to the degree that our ancestors once did" (128) because we now rely on our sight. If sight is so important to humans, evolutionarily speaking, why are there genes that code for color blindness? Is there another selective advantage in those genes that keep them around despite the negatives? Discuss also the structure of the eye and the mechanisms that allow us to see in color. Address also the genetic components of myopia and hyperopia. Why do these defects exist with such prevalence if sight is so important?
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I think that it’s not necessarily an evolutionary advantage for us to be born blind or colourblind, however, it is just a mutation in the gene that codes for sight that causes us to go blind- colorblindness or blindness, if truly a necessity, would’ve been worked into our system by now and no one would care. No, it is a mutation, much like in an animal that relies heavily on smell will have members of its group that have anosmia, which means the sense of smell is lost. Rather, the genes for color blindness either stick around due to their spontaneous mutation or due to the overwhelming adaptions humans have made in conquering them. No longer would it be necessary for us to tell berries apart, or to look where we’re going, as we have machines to do that for us. (posting to get in for Wednesday)
ReplyDeleteThe interior of the eye is lined with a layer of photosensitive cells known collectively as the retina and this is the organ or vision. The eye holds the retina and supplies it with images from the outside world. Light enters the eye through the cornea and the iris and then passes through the lens and then it strikes the retina. The image that is received by the retina is focused by the cornea and the lens. The eye is able to partially adapt to different levels of illumination since the iris can change shape to provide a central hole with a diameter between 2 mm for bright light and 8 mm for dim light. The retina interprets the light into nerve signals and is made up of three nerve-cell bodies. The photosensitive cells, rods and cones, form the layer of cells at the back of the retina. To reach and stimulate the rods and cones, light must pass through the other bodies first. The reasons or this backward-design of the retina are not fully understood but one theory is that the position of the light-sensitive cells at the of the retina allows any stray unabsorbed light to be taken care of by cells immediately behind the retina is melanin. The melanin-containing cells help reimburse the pigments in rods and cones after they have been exposed to light because the rods and cons are highly light sensitive. In the center of the retina are nerve cells which are bilpolar, horizontal, and amacrine cells. . The connectivity of the rods and cones to these three sets of cells is complex but signals eventually pass to the front of the retina and to the third layer of cells known as retinal ganglion cells. The axons from retinal ganglion cells collect in a bundle and leave the eye to form the optic nerve. The backward-design of the retina means that the optic nerve must pass through the retina in order to leave the eye and this results in the so-called blind spot. The rods and cones contain visual pigments. The visual pigments have a special property, however, in that when a visual pigment absorbs a photon of light it changes molecular shape and at the same time releases energy. The pigment in this changed molecular form absorbs light less well than before and thus is often said to have been bleached. The release of energy by the pigment and the change in shape of the molecule together cause the cell to fire, that is to release an electrical signal, by a mechanism that is still not completely understood.
ReplyDeleteAs for the color vision, color vision is a way to differentiate between the wavelengths or frequencies of light that are emitted by a special object. The color is derived from the cone photoreceptors in the eye that the nervous system uses to differentiate. The cone receptors are sensitive to the each part of the visible spectrum. The visible spectrum for humans is to 380 to 740 nm and the eye has cone receptors that are specific to the visible spectrum. The visible spectrum varies between species. A red apple, for example, does not emit red light. The apple, however, absorbs all the light and it only reflects red light. An apple is a good way of shows how our brain is able to differentiate between the different wavelengths; an apple is perceived to be red only because the human eye can distinguish between different wavelengths.
Myopia, which is also known as near-sightedness, is a refractive defect of the eye in which visual images come to a focus in front of the retina, resulting in defective vision of distant objects.People with myopia have a hard time seeing distant objects as they become blurred. In myopia, there are many defects with the eye. The eyeball is too long and the cornea is too steep, so images are not focused on the retina, but instead they are focused on the vitreous inside the eye. Myopia can be genetically inherited and it can be in your genes. Hyperopia is known as farsightedness and it is a type of refractive error which occurs when light enters the eye and the point of focus is behind the retina which results in blurred vision. The hyperopic eye is not able to see the objects that are nearby. This usually occurs when the eyeball is too short or the lens cannot become round enough. In hyperopia images are projected behind the retina. Hyperopia is also genetic and usually happens as you get old. Vision is very important and this defect occurs because this is a random mutation that may have happened. If natural selection were to take its part in this there would be less number of people having this because the people that have myopia or hyperopia would be at a disadvantage and would be at low risk of survival.
http://en.wikipedia.org/wiki/Color_vision
http://en.wikipedia.org/wiki/Hyperopia
http://en.wikipedia.org/wiki/Eye
http://www.softchalk.com/CSExamples/CSExample4/index.html
Wednesday, April 15, 2009
ReplyDeleteColor Blind
On pages 94-98, Carroll discusses the evolution of color vision in humans and on pages 127-129 he discusses the subsequent loss of smell. Carroll states that "we no longer rely on our sense of smell to the degree that our ancestors once did" (128) because we now rely on our sight. If sight is so important to humans, evolutionarily speaking, why are there genes that code for color blindness? Is there another selective advantage in those genes that keep them around despite the negatives? Discuss also the structure of the eye and the mechanisms that allow us to see in color. Address also the genetic components of myopia and hyperopia. Why do these defects exist with such prevalence if sight is so important?
First of all, I’d like to commend anirudh on his amazing description of how the eye works. That was very intense. Anyways, back to getting the bio point…
I would have to remain neutral on Ed’s point however. First of all, I thought that color blindness was attributed to the opsin gene and that it’s nonfunctional led to the loss of full or partial color vision. As Carroll described the owl monkeys, and nocturnal monkey, that have opsin genes that have been mutated to the point where they were rendered useless. So Ed is right when he said that there is a mutation within the gene. There have been numerous experiments that identified that the opsin gene plays an important role in color distinction.
An experiment that duplicated opsin gene that enhanced a female’s color perception played an important role in the mate of choice in the guppy. In guppies, male coloration and female color perception plays an important role in mate choice in the guppy, thus it’s an excellent example of both natural and sexual selection and how it can lead to evolution. They found that there was a high sequence of variability in expanded copy numbers of long wave sensitive opsin genes. Since variability parallels the extreme male color polymorphism within guppy populations, then mate choice has been a major factor driving the coevolution of opsins and male ornaments in these species. In a nut shell they pretty much discovered that the more colorful the male, and the more opsin genes that a female had, which allowed to it be more attuned to different variation of color, the more prone they were to mating. The more opsin genes the female had the more selective they became with their mates which made it a selection process where the most colorful males would be able to reproduce.
What I’m trying to say is that I feel that color blindness is due to the loss of the usage in the opsin gene. There must have been a mutation in the DNA code which ended the RNA transcription polymerase from continuing to read the DNA code, thus stopping the transcribing and making the mRNA a lot shorter. With a shorter mRNA, through the entire process of codons and anticodon, where an anticodon with an amino acid matches up with a codon in a ribosome. An incoming aminoacyte RNA binds to the codon in the A site. The peptide bond formation occurs when the ribosome catalyzes the formation of the peptide bond between the new amino acid and the carboxyl end of the growing polypeptide. The rRNA in the A site is translocated to the P site taking the mRNA along with it. Meanwhile the tRNA in the p site moves to the E site and is released from the ribosome. The ribosome shifts the mRNA by one codon when it tranlocates. The ribosome is then ready for the new aminoacyl tRNA. With a shorter code then the polypeptide chain would be a lot shorter which means that the proteins that could help function to distinguish between colors would be diminished.
Is it bad? Not necessarily. Actually it helps some animals such as the owl monkey that is nocturnal. Being color blind and being able to distinguish between light and dark is all that it really needs to be in order to survive. This way it’s able to distinguish predators and prey more easily allowing surviving and reproducing. Is it bad for humans? Yes, color blind people can drive. They aren’t able to distinguish between green and red lights or color signs that are necessary for safety. However, a color blind marine or special ops agent would be able to penetrate through certain camouflages and enemy camouflage gear so that they would kill them without having to wear bulky night vision goggles and protect freedom all over the world.
Mechanisms that allow us to see color is attributed the nerve, the brain, and the eye. Anirudh P did a very excellent job at describing the parts of the eye that distinguish color and what ,myopia and hyperopia is so I would save you some time and reading and direct your attention to his comment. Thank you, it’s been fun.
http://www.ncbi.nlm.nih.gov/pubmed/17015333
http://en.wikipedia.org/wiki/Color_blindness
I think that it’s not necessarily an evolutionary advantage for us to be born blind or colourblind, however, it is just a mutation in the gene that codes for sight that causes us to go blind- colorblindness or blindness, if truly a necessity, would’ve been worked into our system by now and no one would care. No, it is a mutation, much like in an animal that relies heavily on smell will have members of its group that have anosmia, which means the sense of smell is lost. Rather, the genes for color blindness either stick around due to their spontaneous mutation or due to the overwhelming adaptions humans have made in conquering them. No longer would it be necessary for us to tell berries apart, or to look where we’re going, as we have machines to do that for us, we can rely on others to do things for us to do our high evolvement. It has become unnecessary for us to have all three opsins working at the proper frequencies.
ReplyDeleteOpsins are light-sensitive protein coupled receptors of a protein family of photoreceptors in the eyes. Our cone receptors are labeled beta, gamma, and rho, coding for 400-500 nm, 450-630 nm, and 500-700 nm respectively. When one of the genes that codes for the proteins that compose these opsins has a defect, a mutation, then the opsin won’t relay the proper wavelength or a wavelength at all. In early human life, this would’ve been a problem- colors would’ve been something to heavily rely on when the sense of smell has been diminished, and telling between the vibrant colors could be the difference between a poisonous berry or a delicious one, or perhaps a deliciously poisonous one. In any case, colors are simply not as important now- just as myopia and hyperopia, as previously described as nearsightedness and farsightedness, as well as astigmatism (got two of three of these!), have been conquered by several technological advances- the complete dominance of man means that these traits become not disadvantageous, and thus the traits are allowed to pass on from generation to generation. Technology has done this with out appendix and tonsils as well- things that have become completely unnecessary, and thus we simply remove them, keeping their genetic code in the mix longer and longer. It’s just something that really doesn’t matter anymore.
http://www.allaboutvision.com/conditions/astigmatism.htm
http://en.wikipedia.org/wiki/Hyperopia
http://en.wikipedia.org/wiki/myopia
http://en.wikipedia.org/wiki/opsins