IlMelPers
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB56410 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Melanchra persicariae (dot moth) genome assembly, ilMelPers1
| PRJEB57741 | ENA
Project description:Melanchra persicariae (dot moth), genomic and transcriptomic data
| PRJEB56409 | ENA
Project description:Melanchra persicariae (dot moth) genome assembly, ilMelPers1, alternate haplotype
| PRJEB57742 | ENA
Project description:Methylation of histone H3 at lysine 79 (H3K79) is conserved from yeast to humans and is accomplished by Dot1 (disruptor of telomeric silencing-1) methyltransferases. The C. elegans enzyme DOT-1.1 and its interacting partners are similar to the mammalian DOT1L (Dot1-like) complex. The C. elegans DOT-1.1 complex has been functionally connected to RNA interference. Specifically, we have previously shown that embryonic and larval lethality of dot-1.1 mutant worms deficient in H3K79 methylation was suppressed by mutations in the RNAi pathway genes responsible for generation (rde-4) and function (rde-1) of primary small interfering RNAs (siRNAs). This suggests that dot-1.1 mutant lethality is dependent on the enhanced production of some siRNAs. We have also found that this lethality is suppressed by a loss-of-function of CED-3, a conserved apoptotic protease. Here, we describe a comparison of gene expression and primary siRNA production changes between control and dot-1.1 deletion mutant embryos. We found that elevated antisense siRNA production occurred more often at upregulated than downregulated genes. Importantly, gene expression changes were dependent on RDE-4 in both instances. Moreover, the upregulated group, which is potentially activated by ectopic siRNAs, was enriched in protease-coding genes. Our findings are consistent with a model where in the absence of H3K79 methylation there is a small RNA-dependent activation of protease genes, which leads to embryonic and larval lethality. DOT1 enzymes’ conservation suggests that the interplay between H3K79 methylation and small RNA pathways may exist in higher organisms.
2023-02-02 | GSE223864 | GEO
Project description:Methylation of histone H3 at lysine 79 (H3K79) is conserved from yeast to humans and is accomplished by Dot1 (disruptor of telomeric silencing-1) methyltransferases. The C. elegans enzyme DOT-1.1 and its interacting partners are similar to the mammalian DOT1L (Dot1-like) complex. The C. elegans DOT-1.1 complex has been functionally connected to RNA interference. Specifically, we have previously shown that embryonic and larval lethality of dot-1.1 mutant worms deficient in H3K79 methylation was suppressed by mutations in the RNAi pathway genes responsible for generation (rde-4) and function (rde-1) of primary small interfering RNAs (siRNAs). This suggests that dot-1.1 mutant lethality is dependent on the enhanced production of some siRNAs. We have also found that this lethality is suppressed by a loss-of-function of CED-3, a conserved apoptotic protease. Here, we describe a comparison of gene expression and primary siRNA production changes between control and dot-1.1 deletion mutant embryos. We found that elevated antisense siRNA production occurred more often at upregulated than downregulated genes. Importantly, gene expression changes were dependent on RDE-4 in both instances. Moreover, the upregulated group, which is potentially activated by ectopic siRNAs, was enriched in protease-coding genes. Our findings are consistent with a model where in the absence of H3K79 methylation there is a small RNA-dependent activation of protease genes, which leads to embryonic and larval lethality. DOT1 enzymes’ conservation suggests that the interplay between H3K79 methylation and small RNA pathways may exist in higher organisms.
2023-02-02 | GSE223703 | GEO
Project description:We report the application of a high-throughput technique, RNA-seq, to study the transcriptomic response of P. putida DOT-T1E in the presence of antibiotics with different mechanisms of action with the aim to study in more detail the defense mechanisms that bacteria use to resist against toxic compounds. We find that P. putida DOT-T1E responde in a different way against each antimicrobial compound, what clearly shows that bacteria defense in different ways depending on the targets that compounds uses to attack. Our work is the first global transcriptomic analysis done in P. putida DOT-T1E in the presence of a considerable range of antibiotics. P. putida DOT-T1E mRNA profiles in the presence of control condition (LB) and 8 different antibiotics (ampicillin, chloramphenicol, kanamycin, ciprofloxacin, tetracycline, spectinomycin, gentamicin and rifampicin)
2015-01-20 | E-GEOD-56749 | biostudies-arrayexpress
Project description:We report the application of a high-throughput technique, RNA-seq, to study the transcriptomic response of P. putida DOT-T1E in the presence of antibiotics with different mechanisms of action with the aim to study in more detail the defense mechanisms that bacteria use to resist against toxic compounds. We find that P. putida DOT-T1E responde in a different way against each antimicrobial compound, what clearly shows that bacteria defense in different ways depending on the targets that compounds uses to attack. Our work is the first global transcriptomic analysis done in P. putida DOT-T1E in the presence of a considerable range of antibiotics.
2015-01-20 | GSE56749 | GEO
Project description:Inhibition of transcriptional elongation plays an important role in gene regulation in metazoans, including C. elegans, which lacks Negative Elongation Factor homologs. Here we combine genomic and biochemical approaches to dissect a novel role of C. elegans AF10 homolog, ZFP-1, in transcriptional control. We show that ZFP-1 and its interacting partner DOT-1.1 have a global role in negatively modulating the level of Pol II transcription on essential widely expressed genes. Moreover,the ZFP-1/DOT-1.1 complex contributes to progressive Pol II stalling on essential genes during development and to rapid Pol II stalling during stress response. The slowing down of Pol II transcription by ZFP-1/DOT-1.1 is associated with an increase in H3K79 methylation and a decrease in H2B monoubiquitination, which promotes transcription. We propose a model where recruitment of ZFP-1/DOT-1.1 and deposition of H3K79 methylation at highly expressed genes initiates a negative feedback mechanism for modulation of their expression.
2013-07-05 | GSE47132 | GEO
Project description:Transcriptional control is mediated by interactions of transcription factors with their cognate DNA elements, as well as by epigenetic modifications to chromatin catalyzed by a variety of enzymes. Thus, understanding the crosstalk between transcription factors and epigenetic modifiers is of prime importance. The Dot1-like protein (DOT1L) is an evolutionary conserved methyltransferase with catalytic specificity towards histone 3 lysine 79 (H3K79). DOT1L is essential for mammalian development and has been studied mostly in the context of aggressive leukemias. Recent observations suggest that the role of DOT1L in malignant transformation can be generalized to contexts beyond leukemia. For instance, DOT1L has been implicated in breast cancer progression, and this has been attributed to its cooperation with c-Myc. However, the mechanistic details underlying this association are unknown. Previous work in our lab has shown that DOT-1.1, the C. elegans DOT1L homologue, is recruited to chromatin by ZFP-1 (similarly to DOT1L recruitment by AF10 in mammals), and this complex negatively modulates transcription. Interestingly, promoters of ZFP-1/DOT-1.1 target genes are enriched in E-boxes, the consensus binding motif for c-Myc. Prompted by the exciting hypothesis that DOT-1.1 and MML-1, the C. elegans c-Myc homologue, cooperate genome-wide, we profiled gene expression in wild-type worms and dot-1.1(gk105059), zfp-1(ok554), and mml-1(gk402844) loss-of-function mutants by microarray. We found significant overlaps between genes upregulated in the three mutants, and the same was observed for downregulated genes. A significant global increase of non-coding transcripts was observed in either mutant compared with wild-type. Therefore, ZFP-1/DOT-1.1 and MML-1 co-regulate both coding and non-coding genes and globally inhibit non-coding transcription. Further investigation is underway to uncover the mechanism of cooperation of ZFP-1/DOT-1.1 and MML-1. Profiling of gene expression in wild-type third larval stage (L3) larvae and zfp-1(ok554), dot-1.1(gk105059) and mml-1(gk402844) mutant worms.
2021-09-09 | GSE115677 | GEO