Dataset Information

Hsp90-downregulation influences the heat-shock response, innate immune response and onset of oocyte development in nematodes.

ABSTRACT: Hsp90 is a molecular chaperone involved in the regulation and maturation of kinases and transcription factors. In C. elegans Hsp90 participates in the development of fertility, maintenance of muscle structure and the regulation of stress response and dauer state. To understand the consequences of Hsp90-depletion we studied Hsp90 RNAi-treated nematodes by DNA microarrays and mass spectrometry. We find that upon development of phenotypes the levels of chaperones and cofactors are increased, while specific proteins related to the innate immune response are specifically depleted. We further uncover Hsp90-dependent signatures of gonad development and larval development. Using reporter strains for the responsive genes skr-5, dod-24 and clec-60, we confirm an influence on the innate immune response in intestinal tissues, while alterations to development become evident in strains reporting on the presence of ZIP-8, CAV-1 and SEPA-1 in the gonad arms and very early embryos. These observations add molecular details to the Hsp90-dependent processes during development and stress responses and imply that multiple interactions of this chaperone system are relevant for the nematode’s life and development.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Caenorhabditis Elegans

SUBMITTER: Claudia Lindemann

LAB HEAD: Prof. Dr. Katrin Marcus

PROVIDER: PXD006185 | Pride | 2018-10-17

REPOSITORIES: Pride

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Hsp90-downregulation influences the heat-shock response, innate immune response and onset of oocyte development in nematodes.

Eckl Julia J Sima Siyuan S Marcus Katrin K Lindemann Claudia C Richter Klaus K

PloS one 20171027 10

Hsp90 is a molecular chaperone involved in the regulation and maturation of kinases and transcription factors. In Caenorhabditis elegans, it contributes to the development of fertility, maintenance of muscle structure, the regulation of heat-shock response and dauer state. To understand the consequences of Hsp90-depletion, we studied Hsp90 RNAi-treated nematodes by DNA microarrays and mass spectrometry. We find that upon development of phenotypes the levels of chaperones and Hsp90 cofactors are ...[more]

PMID: 29078207

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Project description:Here we exploit the essential process of X-chromosome dosage compensation to elucidate basic mechanisms that control the assembly, genome-wide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription. ChIP-chip experiments using antibodies against DPY-27, SDC-3, DPY-30, DPY-26, MIX-1, SMC-4, ASH-2 in wild-type embryos. ChIP-chip experiments using antibodies against SDC-3, DPY-27, DPY-30, ASH-2, and IgG in different DCC mutants. ChIP-chip experiments using antibodies against RNA Pol II (hypophosphorylated and S2 and S5) in wild type and sdc-2 partial loss of function mutants.

			Action	DRS
	QEXI08454.mgf	Mgf
	QEXI08454.mzid.gz	Mzid
	QEXI08454.pride.mgf.gz	Mgf
	QEXI08454.raw	Raw
	QEXI08456.mgf	Mgf

Dataset Information

Hsp90-downregulation influences the heat-shock response, innate immune response and onset of oocyte development in nematodes.

Dataset's files

Publications

Hsp90-downregulation influences the heat-shock response, innate immune response and onset of oocyte development in nematodes.

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