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Differential expression of H3.3 genes and their role in modulating temperature stress response in Caenorhabditis elegans

ABSTRACT: Differential expression of H3.3 genes and their role in modulating temperature stress response in Caenorhabditis elegans

PROVIDER: PRJNA418327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6290570.fastq.gz	Fastqsanger.gz
	SRR6290563.fastq.gz	Fastqsanger.gz
	SRR6290564.fastq.gz	Fastqsanger.gz
	SRR6290565.fastq.gz	Fastqsanger.gz
	SRR6290566.fastq.gz	Fastqsanger.gz

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Differential expression of H3.3 genes and their role in modulating temperature stress response in Caenorhabditis elegans

Project description:We generated gene expression profiles of N2 (wild type) and strain FAS43 (Histone H3.3 null worms containing knockout alleles of all genes with homology to human histone H3.3: his-69, his-70, his-71, his-72, his-74) at embryonic and first larval instar stages.

2018-04-19 | GSE106889 | GEO

Loss of histone H3.3 results in DNA replication defects and altered origin dynamics in C. elegans.

Project description:Histone H3.3 is a replication-independent variant of histone H3 with important roles in development, differentiation and fertility. Here we show that loss of H3.3 results in replication defects in Caenorhabditis elegans embryos at elevated temperatures. To characterize these defects, we adapt methods to determine replication timing, map replication origins, and examine replication fork progression. Our analysis of the spatiotemporal regulation of DNA replication shows that despite the very rapid embryonic cell cycle, the genome is replicated from early and late firing origins and is partitioned into domains of early and late replication. We find that under temperature stress conditions, additional replication origins become activated. Moreover, loss of H3.3 results in altered replication fork progression around origins, which is particularly evident at stress-activated origins. These replication defects are accompanied by replication checkpoint activation, a delayed cell cycle, and increased lethality in checkpoint-compromised embryos. Our comprehensive analysis of DNA replication in C. elegans reveals the genomic location of replication origins and the dynamics of their firing, and uncovers a role of H3.3 in the regulation of replication origins under stress conditions.

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Differential Expression of Histone H3.3 Genes and Their Role in Modulating Temperature Stress Response in <i>Caenorhabditis elegans</i>.

Project description:Replication-independent variant histones replace canonical histones in nucleosomes and act as important regulators of chromatin function. H3.3 is a major variant of histone H3 that is remarkably conserved across taxa and is distinguished from canonical H3 by just four key amino acids. Most genomes contain two or more genes expressing H3.3, and complete loss of the protein usually causes sterility or embryonic lethality. Here, we investigate the developmental expression patterns of the five Caenorhabditis elegans H3.3 homologs and identify two previously uncharacterized homologs to be restricted to the germ line. Despite these specific expression patterns, we find that neither loss of individual H3.3 homologs nor the knockout of all five H3.3-coding genes causes sterility or lethality. However, we demonstrate an essential role for the conserved histone chaperone HIRA in the nucleosomal loading of all H3.3 variants. This requirement can be bypassed by mutation of the H3.3-specific residues to those found in H3. While even removal of all H3.3 homologs does not result in lethality, it leads to reduced fertility and viability in response to high-temperature stress. Thus, our results show that H3.3 is nonessential in C. elegans but is critical for ensuring adequate response to stress.

| S-EPMC5972426 | biostudies-literature

Caenorhabditis elegans

Project description:Caenorhabditis elegans Temperature-Sensitive Mutant Collection Genome sequencing

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Light/dark- and temperature-regulated transcriptional rhythms in adult Caenorhabditis elegans

Project description:Most organisms have an endogenous circadian clock that is synchronized to environmental signals such as light and temperature. Although circadian rhythms have been described in the nematode C. elegans at the behavioral level, these rhythms appear to be relatively non-robust. Moreover, in contrast to other animal models, no circadian transcriptional rhythms have been identified. Thus, whether this simple nematode contains a bona fide circadian clock remains an open question. We used microarray experiments to identify light- and temperature-regulated transcriptional rhythms in C. elegans, and show that subsets of these transcripts are regulated in a circadian manner. In addition, we find that light and temperature also globally drive the expression of many genes, indicating that C. elegans exhibits systemic responses to these stimuli.

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Transcriptome analysis of N2 and flp-6 Caenorhabditis elegans at 25 °C

Project description:Temperature is a prominent environmental stimulus that influences life span. Previous studies indicate that in Caenorhabditis elegans, thermosensory perception in the AFD neuron maintains life span at warm temperatures. How thermosensation is translated into neuronal signals that shape aging remains elusive. We found that the Caenorhabditis elegans CREB crh-1, as well as several key genes in AFD thermosensory transduction, were specifically required for normal life span at warm temperatures. crh-1 acted in the AFD to increase transcription of the CRE-containing neuropeptide gene flp-6 in a temperature-dependent manner. Both crh-1 and flp-6 were necessary and sufficient for longevity at warm temperatures, and their effects depended on the AIY interneuron. Moreover, flp-6 signaling downregulated ins-7/insulin and several insulin pathway genes, whose activity compromised life span. We postulate that temperature experience is integrated in the thermosensory neurons to generate CREB-dependent neuropeptide signals that antagonize insulin signaling and promote temperature-specific longevity.

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Transcriptional profiling of Caenorhabditis elegans in control (20°C) and heat shock (35°C) of N2 (WT) and miR-85(n4117) animals

Project description:Transcriptional profiling of N2 (WT) and miR-85(m4117) Caenorhabditis elegans at larval stage 4 (L4) compared at either control temperature (20°C) or after 3hr HS (35°C).

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Variations in diet type and temperature significantly affect the transcriptional profile of C. elegans

Project description:The transcriptomes of model organisms have been defined under specific laboratory growth conditions. The standard protocol for Caenorhabditis elegans growth and maintenance is 20ºC on an Escherichia coli diet. Temperatures ranging from 15ºC to 25ºC or feeding with other species of bacteria are considered physiological lab conditions, but the effect of these conditions on the worm transcriptome have not been well characterized. Here, we compare the global patterns of gene expression for the reference Caenorhabditis elegans strain (N2) grown at 15oC, 20oC, and 25oC on two different diets, Escherichia coli and Bacillus subtilis. When C. elegans were fed E. coli and the growth temperature was increased, we observed an enhancement of defense response pathways and down-regulation of genes associated with metabolic functions. However, when C. elegans were fed B. subtilis and the growth temperature was increased, the nematodes exhibited a decrease in defense response pathways and an enhancement of expression of genes associated with metabolic functions. Our results show that C. elegans undergo significant metabolic and defense response changes when the maintenance temperature fluctuates within the physiologically accepted experimental range and that the degree of pathogenicity of the bacterial diet can further alter the worm transcriptome.

2017-11-02 | GSE101524 | GEO