Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1026370 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26331879_1.fastq.gz | Fastqsanger.gz | |||
| SRR26331879_2.fastq.gz | Fastqsanger.gz | |||
| SRR26331880_1.fastq.gz | Fastqsanger.gz | |||
| SRR26331880_2.fastq.gz | Fastqsanger.gz | |||
| SRR26331881_1.fastq.gz | Fastqsanger.gz |
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Project description:Artemisinin (ARS) displayed bactericidal activity against Vibrio cholerae. To assess the mechanistic details of its antibacterial action, we have isolated V. cholerae mutants with enhanced ARS resistance and identified a gene (VCA0767), whose loss-of-function resulted in the ARS resistance phenotypes. This gene (atrR) encodes a TetR family transcriptional regulator, and its deletion mutant displayed the reduction in ARS-induced ROS formation and DNA damage. Transcriptomic analysis revealed that the genes encoding an RND efflux pump operon (vexRAB) and the outer membrane component (tolC) were highly upregulated in the artR mutant, suggesting that AtrR might act as a negative regulator of this operon and tolC. Gene deletion of vexR, vexB or tolC abrogated the ARS resistance of the atrR mutant and, more importantly, the ectopic expression of VexAB-TolC was sufficient for the ARS resistance, indicating that the increased expression of the VexAB-TolC efflux system is necessary and sufficient for the ARS resistance of the atrR mutant. The cytoplasmic accumulation of ARS was compromised in the vexBtolC mutant, suggesting that the VexAB-TolC might be the primary efflux system exporting ARS to reduce its toxicity inside of the bacterial cells. The atrR mutant displayed resistance to erythromycin as well in a VexR-dependent manner. This result suggests that AtrR may act as a global regulator responsible for preventing intracellular accumulation of toxic chemicals by enhancing the RND efflux system.
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Project description:The identity of most functional elements in the mammalian genome and the phenotypes they impact are unclear. Here, we perform a genome-wide comparative analysis of patterns of accelerated evolution in species with highly distinctive traits to discover candidate functional elements for clinically important phenotypes. We identify accelerated regions (ARs) in the elephant, hibernating bat, orca, dolphin, naked mole rat and thirteen-lined ground squirrel lineages in mammalian conserved regions, uncovering ~33,000 elements that bind hundreds of different regulatory proteins in humans and mice. ARs in the elephant, the largest land mammal, are uniquely enriched at elephant DNA damage response genes and changed conserved regulatory sites. The genomic hotspot for elephant ARs is the E3 ligase subunit of the Fanconi Anemia Complex, a master regulator of DNA repair. Additionally, ARs in the six species are associated with specific human clinical phenotypes that have apparent concordance with overt traits in each species.
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Project description:During angiosperm male gametogenesis, microspores divide to produce a vegetative cell (VC) and a male germline (MG), each with a distinct cell fate. How the MG cell/VC fate is determined remains largely unknown. Here, we report that the VC-targeted H3K27me3 erasure resulted in VC fate transition towards a gamete destination. Multi-omics and cytologic analysis reveal that H3K27me3 is essential for VC fate commitment and contributes to suppress the MG cell fate initiation in VC, whereas MG cells require H3K27me3 reprograming for the gamete cell fate. This work suggests that the MG cell/VC fate is epigenetically regulated. The dimorphic H3K27 methylation acts as a core switch to determine their distinct cell fates and ensure the functional specification of both VC and MG for pollen fertility. This work also provides direct evidences for the proposal that VC maintains the default developmental program of microspore, whereas MG requires reprogramming.
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