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Caenorhabditis elegans AF4/FMR2 family homolog affl-2 regulates heat shock induced gene expression

ABSTRACT: Caenorhabditis elegans AF4/FMR2 family homolog affl-2 regulates heat shock induced gene expression

PROVIDER: PRJNA635013 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11847300.fastq.gz	Fastqsanger.gz
	SRR11847301.fastq.gz	Fastqsanger.gz
	SRR11847302.fastq.gz	Fastqsanger.gz
	SRR11847303.fastq.gz	Fastqsanger.gz
	SRR11847304.fastq.gz	Fastqsanger.gz

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Similar Datasets

Caenorhabditis elegans AF4/FMR2 family homolog affl-2 regulates heat shock induced gene expression

Project description:To mitigate the deleterious effects of temperature increases on cellular organization and proteotoxicity, organisms have developed mechanisms to respond to heat stress. In eukaryotes, HSF1 is the master regulator of the heat shock transcriptional response, but the heat shock response pathway is not yet fully understood. From a forward genetic screen for suppressors of heat shock induced gene expression in Caenorhabditis elegans, we found a new allele of hsf-1 that alters its DNA-binding domain, and we found three additional alleles of sup-45, a previously molecularly uncharacterized genetic locus. We identified sup-45 as one of the two hitherto unknown C. elegans orthologs of the human AF4/FMR2 family proteins, which are involved in regulation of transcriptional elongation rate. We thus renamed sup-45 as affl-2 (AF4/FMR2-Like). Through RNA-seq, we demonstrated that affl-2 mutants are deficient in heat shock induced transcription. Additionally, affl-2 mutants have herniated intestines, while worms lacking its sole paralog (affl-1) appear wild type. AFFL-2 is a broadly expressed nuclear protein, and nuclear localization of AFFL-2 is necessary for its role in heat shock response. affl-2 and its paralog are not essential for proper HSF-1 expression and localization after heat shock, which suggests that affl-2 may function downstream or parallel of hsf-1. Our characterization of affl-2 provides insights into the regulation of heat shock induced gene expression to protect against heat stress.

2020-05-27 | GSE151164 | GEO

<i>Caenorhabditis elegans</i> AF4/FMR2 Family Homolog <i>affl-2</i> Regulates Heat-Shock-Induced Gene Expression.

Project description:To mitigate the deleterious effects of temperature increases on cellular organization and proteotoxicity, organisms have developed mechanisms to respond to heat stress. In eukaryotes, HSF1 is the master regulator of the heat shock transcriptional response, but the heat shock response pathway is not yet fully understood. From a forward genetic screen for suppressors of heat-shock-induced gene expression in Caenorhabditis elegans, we found a new allele of hsf-1 that alters its DNA-binding domain, and we found three additional alleles of sup-45, a previously molecularly uncharacterized genetic locus. We identified sup-45 as one of the two hitherto unknown C. elegans orthologs of the human AF4/FMR2 family proteins, which are involved in regulation of transcriptional elongation rate. We thus renamed sup-45 as affl-2 (AF4/FMR2-Like). Through RNA-seq, we demonstrated that affl-2 mutants are deficient in heat-shock-induced transcription. Additionally, affl-2 mutants have herniated intestines, while worms lacking its sole paralog (affl-1) appear wild type. AFFL-2 is a broadly expressed nuclear protein, and nuclear localization of AFFL-2 is necessary for its role in heat shock response. affl-2 and its paralog are not essential for proper HSF-1 expression and localization after heat shock, which suggests that affl-2 may function downstream of, or parallel to, hsf-1 Our characterization of affl-2 provides insights into the regulation of heat-shock-induced gene expression to protect against heat stress.

| S-EPMC7404228 | biostudies-literature

Differential regulation of HSFA1s and HSFA2 after heat shock in Arabidopsis

2013-04-09 | GSE44655 | GEO

Deciphering RpoD-family sigma factors transcriptional regulatory network highlights their multifaceted roles under heat shock conditions in Salmonella Typhimurium [ChIP-exo]

Project description:We present genome-wide RpoD-family sigma factors (RpoD, RpoS, and RpoH) binding profiles and transcriptome profiles in Salmonella Typhimurium 14028s under both control (37°C) and sublethal heat shock conditions (42°C). These genome-scale experimental data show how three RpoD-family sigma factors simultaneously coordinate many types of cellular processes to orchestrate the overall response of S. Typhimurium to heat stress.

2024-10-20 | GSE266444 | GEO

Deciphering RpoD-family sigma factors transcriptional regulatory network highlights their multifaceted roles under heat shock conditions in Salmonella Typhimurium [RNA-seq]

2024-10-20 | GSE266443 | GEO

MLL-AF4 binds directly to a BCL-2 specific enhancer and impacts H3K27 acetylation

Project description:Survival rates for children diagnosed with acute lymphoblastic leukemia (ALL) have drastically improved, but those carrying mutations in the Mixed Lineage Leukemia (MLL) gene continue to have a very poor prognosis. The most common MLL mutation in ALL is the t(4;11)(q21;q23) chromosome translocation that fuses MLL in frame with the AF4 gene producing MLL-AF4 and AF4-MLL fusion proteins. Previously, we showed that MLL-AF4 binds to the BCL-2 gene and directly activates it through DOT1L recruitment and increased H3K79me2/3 levels. We went on to show that MLL leukemias are particularly sensitive to treatment with the BCL-2 inhibitor venetoclax which synergizes with both standard chemotherapeutic agents as well as DOT1L inhibitors. Altered expression of other BCL-2 family members is a major cause of resistance to ventoclax, so here we perform a detalied analysis of MLL-AF4 regulation of the entire BCL-2 family. By measuring nascent RNA production, we find that of all the BCL-2 family genes, MLL-AF4 directly controls the transcription of both BCL-2 and MCL-1, but only BCL-2 shows a significant loss of steady state RNA levels. Interestingly however, both MCL-1 and BCL-XL protein levels are dependent on MLL-AF4 activity through an unknown and likely indirect mechanism. Finally, we analyze MLL-AF4 regulation of the BCL-2 gene in greater detail and using Capture C we identify a major BCL-2 specific enhancer consisting of two clusters of H3K27Ac. Loss of MLL-AF4 activity results in a reduction of H2K27Ac levels at the major BCL-2 enhancer, revealing a novel regulatory dependence on MLL-AF4 function at BCL-2.

2016-11-23 | GSE85988 | GEO

Transcriptional profiling of Caenorhabditis elegans and Caenorhabditis briggsae before and after heat shock

Project description:Transcriptional profiling of Caenorhabditis elegans and Caenorhabditis briggsae before and after heat shock

| PRJNA560889 | ENA

RNAi-mediated MLL/AF4 knock-down time course

Project description:MLL/AF4 fusion transcript knock-down time course in the MLL/AF4-positive B-cell precursor ALL cell line SEM using MLL/AF4 fusion site-specific siRNAs (siMLL/AF4). The aim was to identify genes responsive to MLL/AF4 expression modulation.

2018-07-21 | GSE71140 | GEO

Differential regulation of HSFA1s and HSFA2 after heat shock in Arabidopsis

Project description:HSFA1s are a gene family of HSFA1 with four members, HSFA1a, HSFA1b, HSFA1d, and HSFA1e. HSFA1s are the master regulators of heat shock response. As a part of the heat shock response, HSFA2 can prolong the heat shock response and amplify the heat shock response in response to repeat heat shock. To identify the heat-shock-responsive genes differentially regulated by HSFA1s and HSFA2, we compared the transcriptomic differences of plants containing only constitutively expressed HSFA1s or HSFA2 after heat stress. hsfa2 (the KO mutant of HSFA2, Col-0 background) and A2QK-10 (CaMV 35S:HSFA2 in QK mutant; QK is HSFA1a/b/d/e quadruple KO mutant) were used to compare the difference of heat shock response when plants lack HSFA1s or HSFA2. The aim is to find the HSFA1s- and HSFA2-preferred regulating genes after heat stress. As the control samples, wild type is the plant with normal heat shock response, and QK (HSFA1s KO mutant, Col-0 and Ws mixed background) is the plant that lost the heat shock response controlled by HSFA1s.

2013-04-09 | E-GEOD-44655 | biostudies-arrayexpress

Change in gene expression in Chlamydomonas reinhardtii upon heat shock

Project description:This was an accompanying experiment. Previously, the expression of genes hsp70A and hsp70B had been established as being tetrapyrrole-dependent (Kropat et al., 1997, 2000). Since both are well-known heat-shock proteins, we performed a one-step heat shock treatment by shifting the temperatures from 23°C to 42°C for 45 min. Moreover, this experiment served as an additional global control to further test the reliability of the microarray and our general conditions since the heat shock response in general is quite well investigated. 3988 responding genes were identified. Among them are 22 genes known to be regulated by HS, selected examples are: the heat shock proteins 22A, 22B and 22C, here leading the list of top-regulated genes on place 1 with a FC of 91297 (22A), place 3 with a FC of 45023 (22B) and place 5 with a FC of 6570 (22C). Other examples are several DnaJ-like proteins or the ClpB chaperone, from the Hsp100 family.

2011-03-02 | GSE20859 | GEO

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