Premium
Endoplasmic Reticulum Stress Induction of Yeast Bax Inhibitor (BXI1) Gene Expression Does Not Entirely Require IRE1
Author(s) -
Finn John Patterson,
Parker Wesley,
Cardona Andrew,
Pineda Edy,
Austriaco Nicanor O.P.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.05982
Subject(s) - endoplasmic reticulum , unfolded protein response , tunicamycin , microbiology and biotechnology , signal transduction , downregulation and upregulation , saccharomyces cerevisiae , biology , gene expression , gene , biochemistry
Bax Inhibitor (BI‐1/TMBIM6) is a regulator protein within the Unfolded Protein Response (UPR) that influences rates of apoptosis within cells. Studies have shown that BI‐1 is upregulated in human cancer cells like prostate and breast, therefore it is important to study the factors that control BI‐1 within a cell. In this paper, the Saccharomyces cerevisiae homolog of BI‐1, BXI1 , is studied to better understand the signaling pathway that influences concentrations of BXI1 , specifically the Inositol Requiring Enzyme 1 ( IRE1 ) pathway. Ire1p is an Endoplasmic Reticulum (ER) bound transmembrane ligand receptor which detects the UPR and activates downstream targets which play further roles in regaining homeostasis. Here, our lab used two genetically modified S. cerevisiae strains, both with Green Fluorescent Protein (GFP) bound to BXI1 (Bxi1p‐GFP) and one lacking genetic information to code for IRE1 (ΔIre1) to test the effect of the IRE1 pathway on the expression of BXI1 . When cells were cultured in media containing either tunicamycin or DDT, we observed an increase in the expression of BXI1 that was not entirely dependent on the IRE1 pathway. This suggests that there may be other signaling pathways that influence the expression of BXI1 . Support or Funding Information Our laboratory is supported by grant NIGMS R15 GM110578, awarded to N. Austriaco.