MicroRNAs acting in a double-negative feedback loop to control a neuronal cell fate decision - PubMed (original) (raw)

Mutations in lsy genes cause a state transition between the ASEL and ASER fates. (A) Gene regulatory factors controlling ASE laterality, as deduced by our previous genetic analysis (–6). The permissively acting, ASEL/R-expressed genes unc-37/Groucho, lin-49, and ceh-36 (4) are left out for clarity. mir-273 likely acts together with other _mir-273_-related miRNAs (D. Didiano and O.H., unpublished data), yet throughout this paper, we only show mir-273 for clarity. (B) ASEL- and ASER-specific cell fate markers and their regulation by lsy genes. ASER-specific expression can be observed with a subfragment from the hen-1 promoter (hen-1ASER::gfp). In all cases, reporter gene expression in ASE was unambiguously determined by using a chromosomally integrated rfp transgene in the genetic background, which is expressed in ASEL/R. Fig. 5, which is published as

supporting information

on the PNAS web site, shows the quantification of data. (C) Summary of the genetic interactions deduced from B. (D) Early bilateral expression of the ASEL inducer lsy-6 and of the ASER inducer cog-1. Early bilateral expression can also be observed for gcy-6, gcy-7, and lim-6 (Fig. 6, which is published as

supporting information

on the PNAS web site, shows the quantification of all observations). *, _gfp-_expressing cells other than ASE, which are out of focus in Right. (E) Even if both ASE neurons are fated to become ASER in class II lsy-6 mutant animals, they initially express both ASEL and ASER markers. See Fig. 6 for quantification of effects.