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Example sentences for: lin-
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Our collective ignorance of the totality of non-coding RNA genes was laid bare by recent work on microRNAs (miRNAs), an abundant family of 21-22 nucleotide non-coding RNAs [ 2 3 ] . The founding members of this family, lin-4 and let-7, were identified through forward analysis of extant Caenorhabditis elegans mutants [ 4 5 ] . Both of these RNAs are post-transcriptional regulators of developmental timing that function by binding to the 3' untranslated regions (3' UTRs) of target genes [ 5 6 7 8 ] . Although they were long regarded as genetic curiosities possibly specific to nematodes, let-7 was subsequently found to be broadly conserved across bilaterian evolution [ 9 ] and miRNA genes are now recognized as a pervasive and widespread feature of animal and plant genomes [ 10 11 12 13 14 15 16 ] .
Antisense RNAs transcribed from loci distinct from their putative targets, such as lin-4 of Caenorhabditis elegans , are generally short and have the potential to form imperfect duplexes with complementary regions of their sense counterparts [ 3].
miR-125 is an apparent homolog of C. elegans lin-4 [ 29 ] , which functions with let-7 to regulate developmental timing in nematodes.
For example, a slimb allele shows defects in centrosome duplication control [ 34 ] , and slimb null cells undergo apoptosis [ 35 ] . Both effects could be explained by a failure to inactivate E2F, as E2F promotes centrosome duplication in mammalian cells [ 36 ] and E2F can induce apoptosis [ 12 ] [ 13 ] . A link between Slimb function and the RB/E2F pathway of cell proliferation control is also suggested by the genetic interaction between the C. elegans slimb ortholog lin-23 and the RBF ortholog lin-35 in which lin-35 function limits the severity of the loss of lin-23 [ 37 ] . Since RBF is an important modifier of E2F activity, perhaps this interaction is a reflection of the action of both Lin-23 and Lin-35 on E2F.
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