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A novel phosphate-starvation response in fission yeast requires the endocytic function of Myosin I (RNA-seq)

ABSTRACT: S. pombe Myosin I (MyoI) plays a key role in cytoskeletal functions, in particular it is part of the endocytotic machinery. Here we show a novel role for MyoI in regulating the response to low phosphate stress. Deletion of MyoI led to an increased proliferation in low phosphate media when compared to a control strain; mutations in other proteins involved in the early steps of endocytosis, such as ARP2 and Sla2/END4, led to the same phenotype. We show that once cells are deprived of phosphate they undergo clear morphological changes, slow down growth but retain viability. This is reminiscent of a quiescence response, and it is completely abolished when MyoI is absent. Transcriptomic analysis revealed a wide perturbation of gene expression upon phosphate starvation, with rapid induction of stress-regulated genes. However, Æmyo1 cells displayed little or negligible effects at gene expression level when they were phosphate-starved. Using a combination of super resolution microscopy and genetic approaches we pinpointed the specific function of MyoI in endocytosis as critical for the response to low phosphate stress. Furthermore, introduction of point-mutated MyoI (with ablated endocytic function) into a ÆmyoI background failed to restore phosphate stress response. Taken together, our data indicate how endocytosis, and in particular MyoI, play a pivotal role in mediating cellular response to nutrients, bridging the external environment and internal molecular functions of the cells.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE65579 | GEO | 2015/09/15

SECONDARY ACCESSION(S): PRJNA274407

REPOSITORIES: GEO

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A novel phosphate-starvation response in fission yeast requires the endocytic function of Myosin I (ChIP-seq)

Project description:S. pombe Myosin I (MyoI) plays a key role in cytoskeletal functions, in particular it is part of the endocytotic machinery. Here we show a novel role for MyoI in regulating the response to low phosphate stress. Deletion of MyoI led to an increased proliferation in low phosphate media when compared to a control strain; mutations in other proteins involved in the early steps of endocytosis, such as ARP2 and Sla2/END4, led to the same phenotype. We show that once cells are deprived of phosphate they undergo clear morphological changes, slow down growth but retain viability. This is reminiscent of a quiescence response, and it is completely abolished when MyoI is absent. Transcriptomic analysis revealed a wide perturbation of gene expression upon phosphate starvation, with rapid induction of stress-regulated genes. However, Æmyo1 cells displayed little or negligible effects at gene expression level when they were phosphate-starved. Using a combination of super resolution microscopy and genetic approaches we pinpointed the specific function of MyoI in endocytosis as critical for the response to low phosphate stress. Furthermore, introduction of point-mutated MyoI (with ablated endocytic function) into a ÆmyoI background failed to restore phosphate stress response. Taken together, our data indicate how endocytosis, and in particular MyoI, play a pivotal role in mediating cellular response to nutrients, bridging the external environment and internal molecular functions of the cells. ChIP-seq analysis of Myo1-GFP genomic binding in control or low phosphate condition

2015-09-15 | E-GEOD-67105 | biostudies-arrayexpress

A novel phosphate-starvation response in fission yeast requires the endocytic function of Myosin I (RNA-seq)

Project description:S. pombe Myosin I (MyoI) plays a key role in cytoskeletal functions, in particular it is part of the endocytotic machinery. Here we show a novel role for MyoI in regulating the response to low phosphate stress. Deletion of MyoI led to an increased proliferation in low phosphate media when compared to a control strain; mutations in other proteins involved in the early steps of endocytosis, such as ARP2 and Sla2/END4, led to the same phenotype. We show that once cells are deprived of phosphate they undergo clear morphological changes, slow down growth but retain viability. This is reminiscent of a quiescence response, and it is completely abolished when MyoI is absent. Transcriptomic analysis revealed a wide perturbation of gene expression upon phosphate starvation, with rapid induction of stress-regulated genes. However, Æmyo1 cells displayed little or negligible effects at gene expression level when they were phosphate-starved. Using a combination of super resolution microscopy and genetic approaches we pinpointed the specific function of MyoI in endocytosis as critical for the response to low phosphate stress. Furthermore, introduction of point-mutated MyoI (with ablated endocytic function) into a ÆmyoI background failed to restore phosphate stress response. Taken together, our data indicate how endocytosis, and in particular MyoI, play a pivotal role in mediating cellular response to nutrients, bridging the external environment and internal molecular functions of the cells. RNA-seq transcriptomic analysis in control and ∆myo1 S.pombe strains comparing gene expression profiles at 4 and 10 hours after phosphate depletion.

2015-09-15 | E-GEOD-65579 | biostudies-arrayexpress

A novel phosphate-starvation response in fission yeast requires the endocytic function of Myosin I (ChIP-seq)

2015-09-15 | GSE67105 | GEO

Gene expression fingerprinting of ameloblasts shows changes in the endocytosis/cytoskeleton interface across stages.

Project description:We used RNA-seq to identify differentially expressed genes across ameloblast stages in rats. We found expression patterns of enamel matrix proteins, ion channels and transporters, and endocytosis regulators such as clathrin to match those found in previous experimental studies on ameloblasts. We hypothesized that ameloblasts change their endocytotic pathways as they progress from stage and stage, and we sought to identify novel patterns in expression of genes at the endocytosis/cytoskeleton interface. We found that maturation ameloblasts preferentially express synaptojanin 1 and intersectin 2 and secretory ameloblasts preferentially express Numb protein and amphiphysin. We also uncovered differential alternative splicing of ECI genes across ameloblast populations. In pointing to endocytotic genes hitherto unexplored in ameloblasts that also regulate cell morphology, this bioinformatics study suggests a mechanism by which cervical loop, secretory, and maturation ameloblasts switch modes of endocytosis in order to express genes that better suit the distinct morphology of each cell stage.

2021-07-14 | GSE133330 | GEO

Role of the extracytoplasmic function sigma factor SigE in the stringent response of Mycobacterium tuberculosis

Project description:Bacteria respond to nutrient starvation implementing the stringent response, a stress signalling system resulting in metabolic remodelling leading to decreased growth rate and energy requirements. A well-characterized model of stringent response in Mycobacterium tuberculosis is that one induced by growth in low phosphate. The extracytoplasmic function (ECF) sigma factor SigE was previously suggested having a key role in the activation of stringent response. In this study we challenge this hypothesis by analyzing the temporal dynamics of the transcriptional response of a sigE mutant and its wild-type parental strain to low phosphate using RNA sequencing. We found that both strains responded to low phosphate with a typical stringent response trait, including the downregulation of genes encoding ribosomal proteins and RNA polymerase. We also observed transcriptional changes that support the occurring of an energetics imbalance, compensated by a reduced activity of the electron transport chain, decreased export of protons and a remodelling of central metabolism. The most striking difference between the two strains was the induction in the sigE mutant of several stress-related genes. In particular, the genes encoding the ECF sigma factor SigH and the transcriptional regulator WhiB6. Since both proteins respond to redox unbalances, their induction suggests that the sigE mutant is not able to maintain redox homeostasis in response to the energetics imbalance induced by low phosphate. In conclusion, our data suggest that SigE is not directly involved in initiating stringent response, but in protecting the cell from stress consequent to the exposure to low phosphate and activation of stringent response.

2022-08-16 | GSE211141 | GEO

RNA-seq analysis of Salmonella enterica Typhimurium LT2

2013-03-26 | GSE45445 | GEO

RNA-seq analysis of Salmonella enterica Typhimurium LT2

Project description:We performed whole-genome transcriptomic analyses of the Salmonella Typhimimurium genome during glucose-phosphate stress. In particular, we wanted to elucidate the role of the the small RNA SgrS and protein regulator SgrT in the stress response. Wild-type Salmonella cells, mutants of Salmonella either lacking sgrS or lacking SgrS RNA/ SgrT peptide function were subject to glucose-phoshate stress

2013-03-26 | E-GEOD-45445 | biostudies-arrayexpress

Quantitative proteomics analysis of soybean leaves under low and high phosphate conditions

Project description:Low phosphate (LP) availability is a critical limiting factor affecting soybean production. Soybean plants develop a series of strategies to adapt phosphate limitation condition. To know the underlying molecular mechanisms responsible for LP stress response. A label-free quantification (LFQ) analysis of soybean leaves grown under low and high phosphate condition was performed.

2021-09-09 | PXD023343 | Pride

The endocytic TPLATE complex internalizes ubiquitinated plasma membrane cargo

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2023-03-11 | PXD035444 | Pride

Phosphate Starvation of Maize Inhibits Lateral Root Formation and Alters Gene Expression in the Lateral Root Primordium Zone

Project description:Low phosphate concentrations are frequently a constraint for maize growth and development, and therefore, enormous quantities of phosphate fertilizer are expended in maize cultivation, which increases the cost of planting. Low phosphate stress not only increases root biomass but can also cause significant changes in root morphology. Low phosphate availability has been found to favor lateral root growth over primary root growth by dramatically reducing primary root length and increasing lateral root elongation and lateral root density in Arabdopsis. While in our assay when inbred line Q319 subjected to phosphate starvation, The numbers of lateral roots and lateral root primordia were decreased after 6 days of culture in a low phosphate solution (LP) compared to plants grown under normal conditions (sufficient phosphate, SP), and these differences were increased associated with the stress caused by phosphate starvation. However, the growth of primary roots appeared not to be sensitive to low phosphate levels. This is very different to Arabidopsis. To elucidate how low phosphate levels regulate root modifications, especially lateral root development, a transcriptomic analysis of the 1.0-1.5 cm lateral root primordium zone (LRZ) of maize Q319 treated after 2 and 8 days by low phosphate was completed respectively. The present work utilized an Arizona Maize Oligonucleotide array 46K version slides, which contained 46,000 maize 70-mer oligonucleotides designated by TIGR ID, and the sequence information is available at the website of the Maize Oligonucleotide Array Project as the search item representing the >30,000 identifiable unique maize genes (details at http://www.maizearray.org). Keywords: low phosphate, Lateral Root Primordium Zone, maize

2012-03-09 | GSE36368 | GEO

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