Our DNA replication machinery is
remarkably accurate and efficient, but errors do occasionally occur. For
example, the same gene may be replicated more than once, resulting in multiple copies of that gene. According to Evan Eichler and his colleagues from
the University of Washington and other institutions, one such duplication event
may have been responsible for the differences between our brains and those of
the great apes.
The original gene, SRGAP2, encodes a protein that is critical for neuronal
development in mammalian embryos. Around the time Australopithecus was evolving into Homo, we ended up with a couple of extra copies of this gene.
Chimps and orangutans each have only one version of the gene, but we have four.
The first duplication (SRGAP2B) probably occurred about 3.4 million years ago (mya), the
next (SRGAP2C, a copy of SRGAP2B), 2.4 mya, and the last (SRGAP2D, also a copy of SRGAP2B) only 1 mya.
Upon reading that humans have extra copies of a gene involved
in neuron maturation, you might think that it’s the excess amounts of this
protein product that lets us be so brainy. Not so. Franck Polleux of the Scripps Research Institute and his colleagues found that the second SRGAP2 duplication (SRGAP2C) encodes a protein that actually interferes with the original gene product. To operate properly, two SRGAP2 proteins must combine together. Because SRGAP2C encodes an incomplete copy, it can pair with the original SRGAP2, but the result is unusable. In other words, thanks to the duplication events, we have less functional SRGAP2 protein,
not more.
The consequence of this is that the developmental schedule of neurons is
altered. With SRGAP2 blocked
during embryogenesis, the period of time allowed for neuronal development is
elongated. This allows for the formation of longer and more numerous neuronal
spines, the parts of the neuron that make connections with other neurons. SRGAP2 also inhibits neural migration, the spreading of neurons throughout the brain. Without it, neurons can continue to migrate for longer. It’s not difficult to see how these changes would have had a huge impact on the evolution of hominin brains.
Think about this: not only were there errors in replicating SRGAP2 millions of years ago, but those errors resulted in a protein product that exactly interfered with the original product. We may very well owe our ability to reason to those serendipitous events. You gotta love evolution.
Think about this: not only were there errors in replicating SRGAP2 millions of years ago, but those errors resulted in a protein product that exactly interfered with the original product. We may very well owe our ability to reason to those serendipitous events. You gotta love evolution.
Hi!
ReplyDeleteA couple of things stand in the way.
Apparently these genes are in a very stable position in different chromosomes. Can there really be that much variability in these genes (If they are in such a stable position)? And, if these mutations minimize the expression of the original gene SRGAP2, wouldn´t our ancestors have more developed and bigger brains?
What about the evoultion-process in other organs? could they all have happened randomly along this SRGAP2 so that a homo sapiens turned out from that?
Thanks for blogging, you really catched my interest!
You're very welcome, and thank you. As to your questions, I'm not sure I completely understand what you're asking. There was an increase in brain size that may correspond with the duplication events. Of course, there would have been other changes that altered other aspects of our ancestors' physiology. More than a single set of gene duplications was required for us to evolve into Homo sapiens.
ReplyDelete