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Candida albicans

ABSTRACT: Candida albicans: response of tor1 mutants to plumbagin, Raw sequence reads

PROVIDER: PRJNA753651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15412757_1.fastq.gz	Fastqsanger.gz
	SRR15412758_1.fastq.gz	Fastqsanger.gz
	SRR15412759_1.fastq.gz	Fastqsanger.gz
	SRR15412760_1.fastq.gz	Fastqsanger.gz
	SRR15412761_1.fastq.gz	Fastqsanger.gz

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Transcript profiling of Candida albicans tor1 kinase mutants

Project description:This study analyses the effects of truncation of the gene encoding Tor1 kinase in Candida albicans. The study involves a mutant tetO-TOR1-Del381 which has the N terminal regulator HEAT repeats deleted compared to a full length tetO-TOR1 strain and a heterozygous TOR1/tor1 control. Cell were grown in vitro in YEPD broth at 30˚C. In shut off experiments, doxycycline (30 µg.ml) was added to cultures to shut off the tetO promoter and inhibit Tor1 expression.

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Project description:Eukaryotic cell growth is coordinated in response to nutrient availability, growth factors, and environmental stimuli, enabling cell–cell interactions that promote survival. The rapamycin-sensitive Tor1 protein kinase, which is conserved from yeasts to humans, participates in a signaling pathway central to cellular nutrient responses. To gain insight into Tor-mediated processes in human fungal pathogens, we have characterized Tor signaling in Candida albicans. Global transcriptional profiling revealed evolutionarily conserved roles for Tor1 in regulating the expression of genes involved in nitrogen starvation responses and ribosome biogenesis. Interestingly, we found that in C. albicans Tor1 plays a novel role in regulating the expression of several cell wall and hyphal specific genes, including adhesins and their transcriptional repressors Nrg1 and Tup1. In accord with this transcriptional profile, rapamycin induced extensive cellular aggregation in an adhesin-dependent fashion. Moreover, adhesin gene induction and cellular aggregation of rapamycin-treated cells were strongly dependent on the transactivators Bcr1 and Efg1. These findings support models in which Tor1 negatively controls cellular adhesion by governing the activities of Bcr1 and Efg1. Taken together, these results provide evidence that Tor1-mediated cellular adhesion might be broadly conserved among eukaryotic organisms.

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