Cell biology, molecular embryology, Lamarckian and Darwinian selection as evolvability.
The evolvability of vertebrate systems involves various mechanisms that eventually generate cooperative and nonlethal functional variation on which Darwinian selection can operate. It is a truism that to get vertebrate animals to develop a coherent machine they first had to inherit the right multicellular ontogeny. The ontogeny of a metazoan involves cell lineages that progressively deny their own capacity for increase and for totipotency in benefit of the collective interest of the individual. To achieve such cell altruism Darwinian dynamics rescinded its original unicellular mandate to reproduce. The distinction between heritability at the level of the cell lineage and at the level of the individual is crucial. However, its implications have seldom been explored in depth. While all out reproduction is the Darwinian measure of success among unicellular organisms, a high replication rate of cell lineages within the organism may be deleterious to the individual as a functional unit. If a harmoniously functioning unit is to evolve, mechanisms must have evolved whereby variants that increase their own replication rate by failing to accept their own somatic duties are controlled. For questions involving organelle origins, see Godelle and Reboud, 1995 and Hoekstra, 1990. In other words, modifiers of conflict that control cell lineages with conflicting genes and new mutant replication rates that deviate from their somatic duties had to evolve. Our thesis is that selection at the level of the (multicellular) individual must have opposed selection at the level of the cell lineage. The metazoan embryo is not immune to this conflict especially with the evolution of set-aside cells and other modes of self-policing modifiers (Blackstone and Ellison, 1998; Ransick et al., 1996. In fact, the conflict between the two selection processes permitted a Lamarckian soma-to-germline feedback loop. This new element in metazoan ontogeny became the evolvability of the vertebrate adaptive immune system and life as we know it now. We offer the hypothesis that metazoan evolution solved this ancient conflict by evolving an immunogenetic mechanism that responds with rapid Lamarckian efficiency by retaining the ancient reverse transcriptase enzyme (RNACopyright DNA copying discovered by Temin in 1959 (see Temin, 1989) and found in 1970 in RNA tumor viruses by Temin and Baltimore), which can produce cDNA from the genome of an RNA virus that infects the cells. It seems that molecular Lamarckism can survive (Lewin, 1993).
Hoenigsberg
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Instituto de Genética Evolutiva y Biologia Molecular, Universidad Manuela Beltrán, Bogotá, DC, Colombia. hoenisbe@umb.edu.co
D000486:Allergy and Immunology / Q000266:history; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D019070:Cell Lineage; D004247:DNA / Q000096:biosynthesis; D019143:Evolution, Molecular; D015322:Gene Rearrangement, B-Lymphocyte; D005803:Genes, Immunoglobulin; D005823:Genetics / Q000266:history; D018858:Germinal Center / Q000276:immunology; D049672:History, 19th Century; D049673:History, 20th Century; D008957:Models, Genetic; D018448:Models, Immunological; D009154:Mutation; D012313:RNA / Q000235:genetics; D012641:Selection, Genetic; D027041:Somatic Hypermutation, Immunoglobulin; D014714:Vertebrates / Q000196:embryology / Q000235:genetics* / Q000276:immunology
D012313:RNA; D004247:DNA