Abstract:
:MicroRNAs (miRNAs) play essential, conserved roles in diverse developmental processes through association with the miRNA-induced silencing complex (miRISC). Whereas fundamental insights into the mechanistic framework of miRNA biogenesis and target gene silencing have been established, posttranslational modifications that affect miRISC function are less well understood. Here we report that the conserved serine/threonine kinase, casein kinase II (CK2), promotes miRISC function in Caenorhabditis elegans. CK2 inactivation results in developmental defects that phenocopy loss of miRISC cofactors and enhances the loss of miRNA function in diverse cellular contexts. Whereas CK2 is dispensable for miRNA biogenesis and the stability of miRISC cofactors, it is required for efficient miRISC target mRNA binding and silencing. Importantly, we identify the conserved DEAD-box RNA helicase, CGH-1/DDX6, as a key CK2 substrate within miRISC and demonstrate phosphorylation of a conserved N-terminal serine is required for CGH-1 function in the miRNA pathway.
journal_name
Proc Natl Acad Sci U S Aauthors
Alessi AF,Khivansara V,Han T,Freeberg MA,Moresco JJ,Tu PG,Montoye E,Yates JR 3rd,Karp X,Kim JKdoi
10.1073/pnas.1509499112subject
Has Abstractpub_date
2015-12-29 00:00:00pages
E7213-22issue
52eissn
0027-8424issn
1091-6490pii
1509499112journal_volume
112pub_type
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