User:Jtwsaddress42/Projects/Project 2/Sections/Chapter 9/The Genomic Consequences Of Cellular Totipotency - Multiple Cell Types, Multiple Body Plans, & Vestigial Genetic Routines

All cells in the animal organism contain the same genome, perhaps with the exception of the unfertilized sperm and eggs which contain a half-set of alleles, but not all populations of cells in the organism are identical. Each of the somatic cells in the developing organism has an initial competence to be induced to commit and differentiate into any number of specific cellular phenotypes. This process of commitment gradually constrains and reduces the totipotency of the cellular mitosis - and, ultimately leads to the final determination the differentiated cellular phenotype and the cessation of the mitotic sequence.

Totipotency is the ability of a cell to give rise to multiple cell types via mitosis, or even ultimately an entire multicellular organism - perhaps even one that metamorphosizes between two life stages. The genomic implications of this are that the genome of a cell possesses much more than it phenotypically expresses at any given point in space and time.

Not only does the genome possess the genes necessary for all the tissue types, but it can carry the genes for instructing the formation of more than just one body plan - a phenomena we clearly witness in the metamorphosis of many organisms from juvenile to adult body plans. Indeed, genome duplication events can facilitate the emergence of multiple body plan routines, if they don't disrupt the already established ontogeny.

The genome can also contain vestigial elements of past body plans that are no longer expressed because they have been developmentally bypassed under the pressures of somatic selection over evolutionary time scales as a result of adaptive changes to the body plan. Vestigial elements can lay dormant for long periods of time in the genome and will eventually accumulate a high mutation load eventually degrading the system, but there is the possibility of their reappearance in ontogeny in response to the right inductive signals.