Chromatin remodelling and antisense-mediated up-regulation of the developmental 
switch gene eud-1 control predatory feeding plasticity

Serobyan, V; Xiao, H; Namdeo, S; Rödelsperger, C; Sieriebriennikov, B; Witte, H; Röseler, W; Sommer, RJ

doi:10.1038/ncomms12337

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Chromatin remodelling and antisense-mediated up-regulation of the developmental switch gene eud-1 control predatory feeding plasticity

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Serobyan, V
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Xiao, H
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Namdeo, S
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Rödelsperger, C
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Sieriebriennikov, B
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Witte, H
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Röseler, W
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Sommer, RJ
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Citation

Serobyan, V., Xiao, H., Namdeo, S., Rödelsperger, C., Sieriebriennikov, B., Witte, H., et al. (2016). Chromatin remodelling and antisense-mediated up-regulation of the developmental switch gene eud-1 control predatory feeding plasticity. Nature Communications, 7: 12337. doi:10.1038/ncomms12337.

Cite as: https://hdl.handle.net/21.11116/0000-000A-8541-6

Abstract

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