Ontology highlight
ABSTRACT:
PROVIDER: PRJNA691742 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13426211_1.fastq.gz | Fastqsanger.gz | |||
| SRR13426211_2.fastq.gz | Fastqsanger.gz | |||
| SRR13426212_1.fastq.gz | Fastqsanger.gz | |||
| SRR13426212_2.fastq.gz | Fastqsanger.gz | |||
| SRR13426213_1.fastq.gz | Fastqsanger.gz |
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Project description:Epistatic transcriptional interations underlying oncogenic genetic interactions (GI) via combinatorial CROP-seq
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Project description:Plants use their endogenous clock to regulate many physiological processes related to their survival and adaptability. GIGANTEA (GI), one of the clock proteins, contributes to the maintenance of circadian period length and amplitude and also regulates flowering time and hypocotyl growth in response to day length. In addition to GI, EARLY FLOWERING 4 (ELF4), another clock regulator, also contributes to these processes. However, little is known about the overall interactions between GI and ELF4 in Arabidopsis. In this study, we investigated the genetic interactions between GI and ELF4 in circadian output regulation. The results show that GI is dominant to ELF4 in flowering time determination, but ELF4 is dominant to GI in hypocotyl growth regulation. Moreover, GI and ELF4 have a synergistic effect on endogenous clock regulation. Further, gene expression profiling of gi-2, elf4, and gi-2 elf4 mutants confirmed that GI and ELF4 had differential dominant effects on circadian physiological outputs at dawn and dusk, respectively. This differential dominance of GI and ELF4 provides a potential means to achieve the diversity in the regulation of circadian physiological outputs including flowering time and hypocotyl growth. The genetic interactions between GI and ELF4 could be time-dependent functional dominance along a day, called temporal dominance hereafter. To test this hypothesis, we performed gene expression profiling of WT, gi-2, elf4 and gi elf4 plants at dawn (ZT1) and dusk (ZT16).
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Project description:Candida albicans is part of the human gastrointestinal (GI) microbiota. To better understand how C. albicans efficiently establishes GI colonisation, we competitively challenged growth of 572 signature-tagged strains (~10% genome coverage), each conditionally overexpressing a single gene, in the murine gut. We identified CRZ2, a transcription factor whose overexpression and deletion respectively increased and decreased early GI colonisation. Using clues from genome-wide expression and gene-set enrichment analyses, we found that the optimal activity of Crz2p occurs under hypoxia at 37°C, as evidenced by both phenotypic and transcriptomic analyses following CRZ2 genetic perturbation. Consistent with early colonisation of the GI tract, we show that CRZ2 overexpression confers resistance to acidic pH and bile salts, suggesting an adaptation to the upper sections of the gut. Genome-wide location analyses revealed that Crz2p directly modulates the expression of many mannosyltransferase- and cell-wall protein-encoding genes, suggesting a link with cell-wall function. We show that CRZ2 overexpression alters cell-wall phosphomannan abundance and increases sensitivity to tunicamycin, suggesting a role in protein glycosylation. Our study reflects the powerful use of gene overexpression as a complementary approach to gene deletion to identify relevant biological pathways involved in C. albicans interaction with the host environment.
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Project description:G protein-coupled receptors (GPCRs) are the largest receptor superfamily that can propagate various extracellular stimulus into cells by coupling with heterotrimeric G proteins. G proteins are divided into four families, Gs, Gi/o, Gq/11 and G12/13, which are responsible for the transduction of discrete downstream signaling pathways. Interestingly, one receptor can couple to more than one G protein subtype with different coupling efficiency or kinetics; coupling with the highest efficiency and/or kinetics is known as ‘primary coupling’ whereas the one with lower efficiency and/or slower kinetics is known as ‘secondary coupling’. Due to its significance in human physiology, there has been a great effort to elucidate the precise mechanism of GPCR-G protein coupling, however, the complex nature of GPCR and G protein interaction raises more unanswered questions. Here, we utilized hydrogen/deuterium exchange mass spectrometry (HDX-MS) to understand the molecular mechanism underlying primary and secondary Gi/o coupling using muscarinic acetylcholine receptor type 2 (M2R) and β2-adrenergic receptor (β2AR) as the primary and secondary Gi/o-coupling receptors, respectively. Results showed the engagement of the distal C-terminus of Gi/o with the receptor differentiates primary and secondary Gi/o couplings. In addition, the interaction between the intracellular loop 2 (ICL2) of the receptor and Gi/o in primary Gi/o coupling is not as critical as in primary Gs coupling.
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Project description:Plants use their endogenous clock to regulate many physiological processes related to their survival and adaptability. GIGANTEA (GI), one of the clock proteins, contributes to the maintenance of circadian period length and amplitude and also regulates flowering time and hypocotyl growth in response to day length. In addition to GI, EARLY FLOWERING 4 (ELF4), another clock regulator, also contributes to these processes. However, little is known about the overall interactions between GI and ELF4 in Arabidopsis. In this study, we investigated the genetic interactions between GI and ELF4 in circadian output regulation. The results show that GI is dominant to ELF4 in flowering time determination, but ELF4 is dominant to GI in hypocotyl growth regulation. Moreover, GI and ELF4 have a synergistic effect on endogenous clock regulation. Further, gene expression profiling of gi-2, elf4, and gi-2 elf4 mutants confirmed that GI and ELF4 had differential dominant effects on circadian physiological outputs at dawn and dusk, respectively. This differential dominance of GI and ELF4 provides a potential means to achieve the diversity in the regulation of circadian physiological outputs including flowering time and hypocotyl growth.
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