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Internal biological mechanisms, called circadian clocks, control the timing of a host of biological functions in organisms from fruit flies to humans. Studies of the molecular basis for this circadian rhythmicity began in the early 1980s in Young’s lab at Rockefeller, and in the labs of Jeffrey C. Hall and Michael Rosbash at Brandeis University. Over the past 30 years, these investigators learned that the circadian clocks of Drosophila melanogaster are formed through the actions of a small group of genes including per (period), tim (timeless), dbt (double-time, casein kinase 1), clk (clock), cyc (cycle), sgg (shaggy), Pdp1 (PAR domain protein 1), vri (vrille), crycryptochrome) and ck2 (casein kinase 2). Mutations in any of these “clock” genes—six of which were first characterized in the Young lab—can lengthen or shorten the period of behavioral, physiological, and molecular circadian rhythms, or abolish the rhythms altogether.
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Sofia Axelrod,Xiaoling Li, Yingwo Sun,Samantha Lincoln,Andrea Terceros, Jenna O'Neil,Zikun Wang,Andrew Nguyen, Aabha Vora,Carmen Spicer, Benjamin Shapiro,Michael W. Young
Social Science Research Network (2021)
biorxiv(2020)
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