Stress, genomes, and evolution.
Evolutionary change, whether in populations of organisms or malignant tumor cells, is contingent on the availability of inherited variation for natural selection to act upon. It is becoming clear that the Hsp90 chaperone, which normally functions to buffer client proteins against the effects of genetic variation, plays a central role in this process. Severe environmental stress can overwhelm the chaperone's buffering capacity, causing previously cryptic genetic variation to be expressed. Recent studies now indicate that in addition to exposing existing variation, Hsp90 can induce novel epigenetic and genetic changes. We discuss key findings that suggest a rich set of pathways by which Hsp90 can mediate the influences of the environment on the genome.
Human Genome Sequencing Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. david.mittelman@bcm.edu
David
D
Mittelman
John H
JH
Wilson
D002460:Cell Line; D019143:Evolution, Molecular; D015894:Genome, Human / Q000235:genetics*; D018841:HSP90 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D053842:Microsatellite Instability; D051135:Rad51 Recombinase / Q000235:genetics / Q000378:metabolism; D013312:Stress, Physiological / Q000235:genetics*; D018911:Trinucleotide Repeats / Q000235:genetics*
D018841:HSP90 Heat-Shock Proteins; C495153:RAD51 protein, human; D051135:Rad51 Recombinase