![]() A brain is still constructed, but it will have different kinds of neural pathways and connections and hence, perhaps, different ways of doing things. For example, if the pioneer neurons in our example carried a switch mutation that prevented them from secreting the nerve growth hormone at the appropriate time, the next phalanx of neurons wouldn't move towards them and might, instead, pick up on a more distant hormonal signal from another brain region and move in that direction, forming synapses with a new set of neurons altogether. When A happens, that allows B and C to happen B allows D and E to happen and so on.īecause brain development is so contingent on what has gone on before, it's pretty easy to alter what happens. Granted that this is an absurdly simplified account of brain development, it suffices to make a key point, which is that brains build themselves. The first to arrive at the pulsating source proceed to form synaptic connections with their targets any laggards, by contrast, fail to proliferate and instead degenerate. As the next phalanx of neurons migrates into the region, they follow the hormone gradient, akin to male moths moving up pheromone gradients to find females, avidly competing for hormones that will enable their proliferation. Neurons that reach a particular destination switch on genes that allow them to secrete a nerve growth hormone. In the developing mammalian brain, for example, neurons migrate up into the cranium, using much the same kind of amoeboid movement that our deep ancestor employed to capture bacteria. Meanwhile, cell #11 expresses a different suite of genes, poising its progeny to influence yet other cells to differentiate into muscle.Īs animals, and hence animal embryos, complexified over time, these cell-to-cell interactions have become increasingly impressive. So, to highly oversimplify the situation, after a fertilized egg has divided into two and then four, then eight, then 16 cells (where the human has, gulp, ten trillion cells), cell #16 makes a regulator that acts to switch on a set of unique genes in cell #10, the outcome being that cell #10 and its progeny eventually give rise to nervous tissue. In addition to being responsive to signals from the environment, they also became responsive to signals coming from their very own cells. In making this transition, animals hung on to the same switch arrangement and the same sets of regulators used by the ancestors, but they added a splendid additional idea. The common-ancestral selves were unicellular, whereas the animal lineage has elected to construct multicellular selves. So, very crudely, the thing on the wall is the switch DNA, your finger is the regulator, and gene expression is the light turning on or turning off. When regulatory molecules bind to this switch DNA, the contiguous gene is either expressed or prevented from being expressed. ![]() Contiguous to each gene is DNA that doesn't code for protein instead, it functions as the gene's on-off switch. Basically, proteins are encoded by sectors of DNA called genes. The way these switches work is pretty straightforward to explain, albeit exquisitely intricate in detail. When things got lean, they instead turned on genes that allowed them to swim off to find new food sources. For example, in the presence of bacterial food, the ancient ancestors turned on the expression of genes that allowed them to crawl around and engulf their prey. Notably, their genomes encoded a rich toolkit of regulatory molecules that turn on or off the expression of genes as appropriate to the occasion. Our single-celled ancestors who lived more than 1.5 billion years ago were already impressively gene-rich and sophisticated, as per last week's blog. To understand their experiments, we first need a crash course in genes and embryos. So, given this, what's the genetic basis for the many ways, notably the cognitive ways, that humans and chimps are different from one another?Ī most ingenious approach to this question is being developed in the lab of Katherine Pollard at the University of California in San Francisco. Moreover, the one percent that are distinctive aren't obviously interesting, being involved with such traits as sperm surface proteins and immune responses. When the protein-encoding genes of the human are compared with the protein-encoding genes of the chimpanzee, they are about 99 percent the same. What's the genetic basis for the many ways that humans and chimps are different from one another?
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