The let-7 microRNA represses the expression of lin-41 to inhibit anterior ventral microtubule (AVM) axon regeneration in older neurons and the effect of let-7 and lin-41 in regulating AVM axon regeneration is mediated through the LIN-29 transcription factor [ 1].
The additional lin-deficient strains are of further importance as they demonstrate varying degrees of acquisition of the lin system and will be useful in future homologous recombination studies to work with manipulated pathway completion through introduction of synthetic lin genes.
Together with the whole-genome analysis suggesting multiple, independent acquisitions of the lin genes, these data suggest that each lin gene has a single evolutionary origin and then is rapidly distributed across species through horizontal transfer events.
The Wnt pathway is also involved in 2° fate specification and appears to act in parallel and through crosstalk with the LIN-12/Notch pathway (Seetharaman et al. 2010).
Likewise, the let-7 microRNA is upstream of lin-41 in the heterochronic pathway and represses LIN-41 translation in hypodermal cells through sequences in the lin-41 3′ UTR, a relationship that is conserved in other systems (Reinhart et al. 2000; Worringer et al. 2014; reviewed by Ecsedi and Grosshans 2013).
(Roslyn Sulcas) 'CROSSING THE LINE': ALEXANDRE ROCCOLI (Tonight through Sunday) Mr. Roccoli opens the dance segment of this multidisciplinary arts festival, produced by the French Institute Alliance Fran?se, with "An Unbecoming Solo".
miRNAs were first found in Caenorhabditis elegans through forward genetic screens of the lin-4 and let-7 mutants [ 9, 10].
Genetic analysis suggests that MISC-1 controls apoptosis through the physiological pathway mediated by the LIN-35/Rb-like protein.
The 22 nt lin-4 transcript temporally negatively regulates translation of lin-14, apparently through antisense RNA-RNA interaction between the lin-4 transcript and multiple regions in the lin-14 3' UTR.
The Lin phenomenon is quickly spreading.
Inhibition of the LIN-53-containing PRC2 through RNAi against mes-2 (EZH2), mes-3 or mes-6 (EED) abolished H3K27 methylation and similarly enabled CHE-1 to convert germ cells to ASE neurons [ 67].
