ArticleGenetics2011
The putative lipid transporter, Arv1, is required for activating pheromone-induced MAP kinase signaling in Saccharomyces cerevisiae.
Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- An Erg11 lanosterol 14-α-demethylase-Arv1 complex is required for Candida albicans virulence.PloS one · 2020Article
- Mice lackingThe Journal of biological chemistry · 2018Article
- A link between very long chain fatty acid elongation and mating-specific yeast cell cycle arrest.Cell cycle (Georgetown, Tex.) · 2017Article
- Proper Sterol Distribution Is Required forG3 (Bethesda, Md.) · 2016Article
- Neuronal deficiency of ARV1 causes an autosomal recessive epileptic encephalopathy.Human molecular genetics · 2016Article
- Arv1 promotes cell division by recruiting IQGAP1 and myosin to the cleavage furrow.Cell cycle (Georgetown, Tex.) · 2016Article
- Ceramide signals for initiation of yeast mating-specific cell cycle arrest.Cell cycle (Georgetown, Tex.) · 2016Article
- Deletion of murine Arv1 results in a lean phenotype with increased energy expenditure.Nutrition & diabetes · 2015Article
- Arv1 regulates PM and ER membrane structure and homeostasis but is dispensable for intracellular sterol transport.Traffic (Copenhagen, Denmark) · 2013Article
- Arv1 lipid transporter function is conserved between pathogenic and nonpathogenic fungi.Fungal genetics and biology : FG & B · 2012Article
- Arv1; a "Mover and Shaker" of Subcellular Lipids.Contact (Thousand Oaks (Ventura County, Calif.))Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Saccharomyces cerevisiae haploid cells respond to extrinsic mating signals by forming polarized projections (shmoos), which are necessary for conjugation. We have examined the role of the putative lipid transporter, Arv1, in yeast mating, particularly the conserved Arv1 homology domain (AHD) within Arv1 and its role in this process. Previously it was shown that arv1 cells harbor defects in sphingolipid and glycosylphosphatidylinositol (GPI) biosyntheses and may harbor sterol trafficking defects. Here we demonstrate that arv1 cells are mating defective and cannot form shmoos. They lack the ability to initiate pheromone-induced G1 cell cycle arrest, due to failure to polarize PI(4,5)P(2) and the Ste5 scaffold, which results in weakened MAP kinase signaling activity. A mutant Ste5, Ste5(Q59L), which binds more tightly to the plasma membrane, suppresses the MAP kinase signaling defects of arv1 cells. Filipin staining shows arv1 cells contain altered levels of various sterol microdomains that persist throughout the mating process. Data suggest that the sterol trafficking defects of arv1 affect PI(4,5)P(2) polarization, which causes a mislocalization of Ste5, resulting in defective MAP kinase signaling and the inability to mate. Importantly, our studies show that the AHD of Arv1 is required for mating, pheromone-induced G1 cell cycle arrest, and for sterol trafficking.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.