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Shoddy Engineering or Intelligent Design? Case of the Mouse’s Eye

We often hear from Darwinians that the biological world is replete with examples of shoddy engineering, or, as they prefer to put it, bad design. One such case of really poor construction is the inverted retina of the vertebrate eye. As we all know, the retina of our eyes is configured all wrong because the cells that gather photons, the rod photoreceptors, are behind two other tissue layers. Light first strikes the ganglion cells and then passes by or through the bipolar cells before reaching the rod photoreceptors. Surely, a child could have arranged the system better — so they tell us.

The problem with this story of supposed unintelligent design is that it is long on anthropomorphisms and short on evidence. Consider nocturnal mammals. Night vision for, say, a mouse is no small feat. Light intensities during night can be a million times less than those of the day, so the rod cells must be optimized — yes, optimized — to capture even the few stray photons that strike them. Given the backwards organization of the mouse’s retina, how is this scavenging of light accomplished? Part of the solution is that the ganglion and bipolar cell layers are thinner in mammals that are nocturnal. But other optimizations must also occur. Enter the cell nucleus and “junk” DNA.

Only around 1.5 percent of mammalian DNA encodes proteins. Since it has become lore to equate protein-coding regions of the genome with “genes” and “information,” the remaining approximately 98.5 percent of DNA has been dismissed as junk. Yet, for what is purported to be mere genetic gibberish, it is strikingly ordered along the length of the chromosome. Like the barcodes on consumer items that we are all familiar with, each chromosome has a particular banding pattern. This pattern reflects how different types of DNA sequences are linearly distributed. The “core” of a mammalian chromosome, the centromere, and the genomic segments that frame it largely consist of long tracks of species-specific repetitive elements — these areas give rise to “C-bands” after a chemical stain has been applied. Then, alternating along the chromosome arms are two other kinds of bands that appear after different staining procedures. One called “R-bands” is rich in protein-coding genes and a particular class of retrotransposon called SINEs (for Short Interspersed Nuclear Elements). SINE sequence families are restricted to certain taxonomic groups. The other is termed “G-bands” and it has a high concentration of another class of retrotransposon called LINEs (for Long Interspersed Nuclear Elements), that can also be used to distinguish between species. Finally, the ends of the chromosome, telomeres, are comprised of a completely different set of repetitive DNA sequences.

In general, C-bands and G-bands are complexed with proteins and RNAs to give a more compact organization called heterochromatin, whereas R-bands have a more open conformation referred to as euchromatin.
Why bother with such details? Well, each of these chromosome bands has a preferred location in the cell nucleus. Open any good textbook on mammalian anatomy and you will note that cell types can often be distinguished by the shape and size of the nucleus, as well as the positions of euchromatin and heterochromatin in that organelle. Nevertheless, most cell nuclei follow a general rule where euchromatin is located in the interior, in various compartments that are dense with transcription factories, RNA processing machinery, and many other components. Heterochromatin, on the other hand, is found mainly around the periphery of the nucleus. A striking exception to this principle is found in the nuclei of rod cells in nocturnal mammals.

Reporting in the journal Cell, Irina Solovei and coworkers have just discovered that, in contrast to the nucleus organization seen in ganglion and bipolar cells of the retina, a remarkable inversion of chromosome band localities occurs in the rod photoreceptors of mammals with night vision (Solovei I, Kreysing M, Lanctôt C, Kösem S, Peichl L, Cremer T, Guck J, Joffe B. 2009. “Nuclear Architecture of Rod Photoreceptor Cells Adapts to Vision in Mammalian Evolution.” Cell 137(2): 356-368). First, the C-bands of all the chromosomes including the centromere coalesce in the center of the nucleus to produce a dense chromocenter. Keep in mind that the DNA backbone of this chromocenter in different mammals is repetitive and highly species-specific. Second, a shell of LINE-rich G-band sequences surrounds the C-bands. Finally, the R-bands including all examined protein-coding genes are placed next to the nuclear envelope. The nucleus of this cell type is also smaller so as to make the pattern more compact. This ordered movement of billions of basepairs according to their “barcode status” begins in the rod photoreceptor cells at birth, at least in the mouse, and continues for weeks and months.
Why the elaborate repositioning of so much “junk” DNA in the rod cells of nocturnal mammals? The answer is optics. A central cluster of chromocenters surrounded by a layer of LINE-dense heterochromatin enables the nucleus to be a converging lens for photons, so that the latter can pass without hindrance to the rod outer segments that sense light. In other words, the genome regions with the highest refractive index — undoubtedly enhanced by the proteins bound to the repetitive DNA — are concentrated in the interior, followed by the sequences with the next highest level of refractivity, to prevent against the scattering of light. The nuclear genome is thus transformed into an optical device that is designed to assist in the capturing of photons. This chromatin-based convex (focusing) lens is so well constructed that it still works when lattices of rod cells are made to be disordered. Normal cell nuclei actually scatter light.

So the next time someone tells you that it “strains credulity” to think that more than a few pieces of “junk DNA” could be functional in the cell — that the data only point to the lack of design and suboptimality — remind them of the rod cell nuclei of the humble mouse.

Richard Sternberg

Senior Fellow, Center for Science and Culture
Richard Sternberg is an evolutionary biologist with interests in the relation between genes and morphological homologies, and the nature of genomic “information.” He holds two Ph.D.'s: one in Biology (Molecular Evolution) from Florida International University and another in Systems Science (Theoretical Biology) from Binghamton University. From 2001-2007, he served as a staff scientist at the National Center for Biotechnology Information, and from 2001-2007 was a Research Associate at the Smithsonian’s National Museum of Natural History. Dr. Sternberg is presently a research scientist at the Biologic Institute, supported by a research fellowship from the Center for Science and Culture at Discovery Institute. He is also a Research Collaborator at the National Museum of Natural History.



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