We thus asked whether miR-71 was required for the reinitiation of developmental programs during the recovery phase after L1 starvation. These results suggest that miR-71 regulates the expression of unc-31 and age-1 through their 3′UTRs. Note that there are extra GFP-positive cells (red arrows) in mir-71(lf) mutants.
- A recent study showed that the expression of miR-71 was significantly increased relative to other miRNAs in starved L1 worms (15).
- To understand how miR-71 affects VPC division, we searched its predicted targets for potential genes involved in regulating developmental timing.
- (A) Differential interference contrast (DIC) images showing L4 worms recovered from 4-d–starved L1 worms.
- On one hand, we showed that deletions of a good number of miRNAs have varying impacts on the L1 diapause survival rate, although they may effect the rate through different mechanisms.
- These results indicate that miR-71 is not essential for arresting seam cell or M-cell divisions during L1 diapause, suggesting that miR-71 function is distinct from DAF-16 function.
- To test the hypothesis that these developmental timing genes mediate the regulatory role of miR-71 in larval development during recovery from starvation-induced L1 diapause, we examined whether knocking down HBL-1 function can suppress the retarded VPC timing defect of mir-71(lf).
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MiR-71 regulates vulval cell division during recovery of starved L1 worms. These results indicate that miR-71 is not essential for arresting seam cell or M-cell divisions during L1 diapause, suggesting that miR-71 function is distinct from DAF-16 function. DAF-16 (the FOXO homolog in C. elegans) has been shown to play an important role in cell cycle arrest and developmental progression partly by promoting cki-1 expression in some somatic cells during L1 arrest (2).
