STE2 encodes a component of the S. cerevisiae alpha-pheromone receptor that is essential for induction of physiological changes associated with mating. Analysis of C-terminal truncation mutants of STE2 demonstrated that the essential sequences for ligand binding and signal transduction are included within a region containing seven putative transmembrane domains. However, truncation of the C-terminal 105 amino acids of the receptor resulted in a 4- to 5-fold increase in cell-surface pheromone binding sites, a 10-fold increase in pheromone sensitivity, a defect in recovery of cell division after pheromone treatment, and a defect in pheromone-induced morphogenesis. Overproduction of STE2 resulted in about a 6-fold increase in alpha-pheromone binding capacity but did not produce the other phenotypes associated with the ste2-T326 mutant receptor. We conclude that the C-terminus of the receptor is responsible for one aspect of cellular adaptation to pheromone that is distinct from adaptation controlled by the SST2 gene, for decreasing the stability of the receptor, and for some aspect of cellular morphogenesis.
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http://dx.doi.org/10.1016/s0092-8674(88)80005-9 | DOI Listing |
is a commonly used microorganism in the biotechnological industry. For the industrial heterologous production of compounds, it is of great advantage to work with growth-controllable yeast strains. In our work, we utilized the natural pheromone system of and generated a set of different strains possessing an α-pheromone controllable growth behavior.
View Article and Find Full Text PDFACS Synth Biol
January 2023
State Key Laboratory of Microbial Technology, Shandong University, No. 72 Binhai Road, Qingdao 266237, P. R. China.
Engineering dynamic control of gene expression is desirable because many engineered functions interfere with endogenous cellular processes that have evolved to facilitate growth and survival. Minimizing conflict between growth and production phases can therefore improve product titers in microbial cell factories. We developed an autoinduced gene expression system by rewiring the pheromone response pathway.
View Article and Find Full Text PDFNat Microbiol
September 2019
Departamento de Genética, Campus de Excelencia Internacional Agroalimentario ceiA3, Universidad de Córdoba, Córdoba, Spain.
Autocrine self-signalling via secreted peptides and cognate receptors regulates cell development in eukaryotes and is conserved from protozoans to mammals. In contrast, secreted peptides from higher fungi have been traditionally associated with paracrine non-self-signalling during sexual reproduction. For example, cells of the model fungus Saccharomyces cerevisiae fall into two distinct mating types (MAT), which produce either a- or α-pheromone and the cognate receptors Ste2 or Ste3, respectively.
View Article and Find Full Text PDFJ Microbiol Biotechnol
September 2018
Department of Molecular Bioscience, College of Biomedical Science, Kangwon National University, Chuncheon 24341, Republic of Korea.
Transcriptional gene silencing is regulated by the chromatin structure, which is by various factors including histones. contains transcriptionally silenced regions such as telomeric regions and hidden mating (HM) loci. The positively-charged amino acids on the histone H4 tail were reported to be critical for the telomeric silencing in yeast, by interacting with Dot1, a specific methyltransferase for the 79.
View Article and Find Full Text PDFFront Microbiol
June 2018
Departamento de Bioquímica y Biología Estructural, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Although most antibiotics act on cells that are actively dividing and non-dividing cells such as in microbe sporulation or cancer stem cells represent a new paradigm for the control of disease. In addition to their relevance to health, such antibiotics may promote our understanding of the relationship between the cell cycle and cell death. No antibiotic specifically acting on microbial cells arrested in their cell cycle has been identified until the present time.
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