Casein kinase II promotes target silencing by miRISC through direct phosphorylation of the DEAD-box RNA helicase CGH-1.
Proc Natl Acad Sci U S A
; 112(52): E7213-22, 2015 Dec 29.
Article
in En
| MEDLINE
| ID: mdl-26669440
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.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
RNA Nucleotidyltransferases
/
Caenorhabditis elegans Proteins
/
RNA-Induced Silencing Complex
/
MicroRNAs
/
RNA Interference
/
Casein Kinase II
Limits:
Animals
Language:
En
Year:
2015
Type:
Article