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Transcriptomic analysis of pals-25(icb98gf) mutants in C. elegans

ABSTRACT: We used RNA-seq to identify gene expression changes in C. elegans pals-25(icb98gf) mutants

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE206756 | GEO | 2022/09/02

REPOSITORIES: GEO

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Transcriptomic analysis of pals-22 and pals-25 mutants in C. elegans

Project description:We used RNA-seq to identify gene expression changes in C. elegans pals-22 mutants, pals-22 pals-25 double mutants, and pals-25 mutants

2022-09-02 | GSE212552 | GEO

Multiple pals gene modules control a balance between immunity and development in Caenorhabditis elegans [RNA-Seq 2]

Project description:The immune system continually battles against pathogen-induced pressures, which often leads to the evolutionary expansion of immune gene families in a species-specific manner. For example, the pals gene family expanded to 39 members in the Caenorhabditis elegans genome, in comparison to a single mammalian pals ortholog. Our previous studies have revealed that two members of this family, pals-22 and pals-25, act as antagonistic paralogs to control the Intracellular Pathogen Response (IPR). The IPR is a protective transcriptional response, which is activated upon infection by two molecularly distinct natural intracellular pathogens of C. elegans – the Orsay virus and the fungus Nematocida parisii from the microsporidia phylum. In this study, we identify a previously uncharacterized member of the pals family, pals-17, as a newly described negative regulator of the IPR. pals-17 mutants show constitutive upregulation of IPR gene expression, increased immunity against intracellular pathogens, as well as impaired development and reproduction. We also find that two other previously uncharacterized pals genes, pals-20 and pals-16, are positive regulators of the IPR, acting downstream of pals-17. These positive regulators reverse the effects caused by the loss of pals-17 on IPR gene expression, immunity and development. We show that the negative IPR regulator protein PALS-17 and the positive IPR regulator protein PALS-20 colocalize inside intestinal epithelial cells, which are the sites of infection for IPR-inducing pathogens. In summary, our study demonstrates that several pals genes from the expanded pals gene family act as ON/OFF switch modules to regulate a balance between organismal development and immunity against natural intracellular pathogens in C. elegans.

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Multiple pals gene modules control a balance between immunity and development in Caenorhabditis elegans [RNA-Seq 1]

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Transcriptomic Analysis of the Intracellular Pathogen Response (IPR)

Project description:We used RNA-seq to identify gene expression changes in C. elegans pals-22 and pals-22 pals-25 mutants compared to wild-type animals, as well as in wild-type animals in response to bortezomib treatment.

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Expression analysis of Caenorhabditis elegans Bristol N2 rsd-2 and rsd-6 single mutants at 25°C and 20°C

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Transcriptomic Analysis of pnp-1 mutants in C. elegans

Project description:We used RNA-seq to identify gene expression changes in C. elegans pnp-1 mutants

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Transcriptomic analysis of C. elegans mutants which fail to activate the oomycete recognition response

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A cullin-RING ubiquitin ligase promotes thermotolerance as part of the Intracellular Pathogen Response in C. elegans.

Project description:Intracellular pathogen infection leads to proteotoxic stress in host organisms. Previously we described a physiological program in the nematode C. elegans called the Intracellular Pathogen Response (IPR), which promotes resistance to proteotoxic stress and appears to be distinct from canonical proteostasis pathways. The IPR is controlled by PALS-22 and PALS-25, proteins of unknown biochemical function, which regulate expression of genes induced by natural intracellular pathogens. We previously showed that PALS-22 and PALS-25 regulate the mRNA expression of the predicted ubiquitin ligase component cullin cul-6, which promotes thermotolerance in pals-22 mutants. However, it was unclear whether CUL-6 acted alone, or together with other cullin-ring ubiquitin ligase components, which comprise a greatly expanded gene family in C. elegans. Here we use co-immunoprecipitation studies paired with genetic analysis to define the cullin-RING ligase components that act together with CUL-6 to promote thermotolerance. First, we identify a previously uncharacterized RING domain protein in the TRIM family we named RCS-1, which acts as a core component with CUL-6 to promote thermotolerance. Next, we show that the Skp-related proteins SKR-3, SKR-4 and SKR-5 act redundantly to promote thermotolerance with CUL-6. Finally, we screened F-box proteins that co-immunoprecipitate with CUL-6 and find that FBXA-158 and FBXA-75 promote thermotolerance. In summary, we have defined the three core components and two F-box adaptors of a cullin-RING ligase complex that promotes thermotolerance as part of the IPR in C. elegans, which adds to our understanding of how organisms cope with proteotoxic stress.

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