Chromatin remodelling and antisense-mediated up-regulation of the developmental switch gene eud-1 control predatory feeding plasticity
Structural plasticity
DOI:
10.1038/ncomms12337
Publication Date:
2016-08-04T09:46:50Z
AUTHORS (8)
ABSTRACT
Phenotypic plasticity has been suggested to act through developmental switches, but little is known about associated molecular mechanisms. In the nematode Pristionchus pacificus, sulfatase eud-1 was identified as part of a switch controlling mouth-form governing predatory versus bacteriovorous decision. Here we show that mutations in conserved histone-acetyltransferase Ppa-lsy-12 and methyl-binding-protein Ppa-mbd-2 mimic phenotype, resulting absence one mouth-form. Mutations both genes cause histone modification defects reduced expression. Surprisingly, mutants also result down-regulation an antisense-eud-1 RNA. are co-expressed further experiments suggest acts itself. Indeed, overexpression RNA increases eud-1-sensitive extends contrast, this effect absent indicating positively regulates eud-1. Thus, chromatin remodelling antisense-mediated up-regulation control feeding Pristionchus.
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