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SUMMARY:Mutation, drift, and the origin of subcellular features
LOCATION:Anatomy/Zoology Building W118
TZID:America/Denver
DTSTART:20122001T000000
UID:2026-04-07-21-08-09@natsci.colostate.edu
DTSTAMP:20260407T210809
Description:Understanding the mechanisms of evolution and the degree to whi
 ch phylogenetic generalities exist requires information on the rate at whi
 ch mutations arise and their effects at the molecular and phenotypic level
 s. Although procuring such data has been technically challenging\, high-th
 roughput genomic sequencing is rapidly expanding our knowledge in this are
 a. Most notably\, information on spontaneous mutations\, now available in 
 a wide variety of organisms\, implies an inverse scaling of the mutation r
 ate (per nucleotide site) with the effective population size of a lineage.
  This pattern appears to arise naturally as natural selection pushes the m
 utation rate down to a lower limit set by the power of random genetic drif
 t rather than by intrinsic molecular limitations on repair mechanisms. Sup
 port for this idea derives from the relative levels of efficiency of DNA p
 olymerases and mismatch-repair enzymes in eukaryotes relative to prokaryot
 es. This drift-barrier hypothesis has general implications for all aspects
  of evolution\, including the performance of enzymes and the stability of 
 proteins. The fundamental assumption is that as molecular adaptations beco
 me more and more refined\, the room for subsequent improvement becomes dim
 inishingly small. If this hypothesis is correct\, the population-genetic e
 nvironment imposes a fundamental constraint on the level of perfection tha
 t can be achieved by any molecular adaptation. It also implies that effect
 ive neutrality is the expected outcome of natural selection\, an idea firs
 t suggested by Hartl et al. in 1985. Although generally viewed as an indep
 endent process\, mutation also operates as a weak selective force\, thereb
 y playing a central role in \"nearly neutral\" hypotheses in evolution. Mo
 st notably\, genes and proteins with more complex structures are subject t
 o higher rates of mutational degeneration simply because they are larger m
 utational targets. However\, because the mutation rate is very low at the 
 nucleotide level\, the efficiency of such mutation-associated selection be
 comes of diminishing significance in populations with small effective size
 s. Thus\, mutationally hazardous genomic and gene-structural features\, wh
 ich may or may not be adaptive\, are expected to passively arise in lineag
 es with small effective sizes. This general principle\, the mutational-haz
 ard theory\, will be illustrated with examples including: 1) the different
 ial expansion of intron numbers in various phylogenetic lineages\; and 2) 
 the diversification of protein-architectural features. 4:00 pm
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