Pah1p negatively regulates the expression of V-ATPase genes as well as vacuolar acidification.

Biochem Biophys Res Commun

Department of Biology, College of Staten Island, City University of New York, 2800 Victory Blvd, Staten Island, NY 10314, United States; PhD Program in Biology, The Graduate Center, City University of New York, 365 Fifth Avenue, New York 10016, United States; Institute for Macromolecular Assemblies, City University of New York, 160 Convent Avenue, New York, NY 10031, United States. Electronic address:

Published: September 2017

In yeast, PAH1 plays an important role in cell homeostasis and lipid biosynthesis. PAH1 encodes for the PA phosphatase, Pah1p, which is responsible for de novo TAG and phospholipid synthesis. It has been suggested that the lack of Pah1p causes irregular vacuolar morphology and dysfunctional V-ATPase pump activity. However, the molecular connection between Pah1p and V-ATPase activity has remained unclear. Through real-time PCR, we have shown that PAH1 is maximally induced at the stationary stage in the presence of inositol. We also found that vacuoles were less fragmented when PAH1 is maximally expressed. Subsequently, we observed that vacuoles from pah1Δ cells were more acidic than those in WT cells. Furthermore, V-ATPase genes were upregulated in the absence of Pah1p. These results suggest that Pah1p plays an important role in vacuolar activity by negatively regulating the expression of V-ATPase genes. As such, we provide evidence to show the role of Pah1p in vacuolar acidification and fragmentation.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2017.07.127DOI Listing

Publication Analysis

Top Keywords

v-atpase genes
12
expression v-atpase
8
vacuolar acidification
8
plays role
8
pah1 maximally
8
pah1p
7
v-atpase
5
pah1p negatively
4
negatively regulates
4
regulates expression
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!