Sternberg needs to write a book debunking junk DNA.
Shoddy Engineering or Intelligent Design? Case of the Mouse’s Eye
By Richard Sternberg
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.
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).
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.