February 7–12, 2012 Fairmont Hotel Vancouver, Vancouver, B.C. Canada
Yu-De and I tried to sell the RACK1 story.
We met 沈湯龍 and 朱家瑩老師！
RACK-1 as a bifunctional factor in the let-7 miRNA pathway
Yu-De Chu1, Shih-Peng Chan1,2* and Frank Slack2*
1Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan
2Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520, USA
The Receptor of Activated C Kinase (RACK-1) has been previously shown as an interactor of miRISC in C. elegant and human. It was proposed that RACK-1 contributes to the recruitment of miRISC to the active ribosomes and repression of RACK-1 may impair miRNA function. In C. elegans, the let-7 miRNA regulates the exit of cell cycle and terminal differentiation. Dysfunction of let-7 results in irregular hypodermal and vulval development. Here we examined the effects of repression of RACK-1 on let-7 function using the wild-type let-7 allele and a ts mutant let-7 allele that expresses a lower amount of let-7. Indeed, in wild-type worms we observed a small fraction of animals showing let-7 defect phenotypes, as shown in the previous studies. However, interestingly, we found that repression of RACK-1 significantly suppressed the defect phenotypes of the ts let-7(n2853) allele. Moreover, repression of RACK-1 resulted in increased levels of let-7 in both wild-type or let-7(n2853) mutant worms. Our results suggest that beside contributing to the recruitment of miRISC, RACK-1 alters the let-7 level via an unknown mechanism. *corresponding authors
Also, we have some easy time there!