Mouse Pxt1 gene is expressed exclusively in male germ cells and encodes for a small, cell death inducing protein. However, upon PXT1 interaction with BAG6, cell death is prevented. In transiently transfected cell lines the PXT1 expression triggered massive cell death, thus we ask the question whether the interaction of PXT1 and BAG6 is the only mechanism preventing normal, developing male germ cells from being killed by PXT1. The Pxt1 gene contains a long 3'UTR thus we have hypothesized that Pxt1 can be regulated by miRNA. We have applied Pxt1 knockout and used Pxt1 transgenic mice that overexpressed this gene to shed more light on Pxt1 regulation. Using the ELISA assay we have demonstrated that PXT1 protein is expressed in adult mouse testis, though at low abundance. The application of dual-Glo luciferase assay and the 3'UTR cloned into p-MIR-Glo plasmid showed that Pxt1 is regulated by miRNA. Combining the use of mirDB and the site-directed mutagenesis further demonstrated that Pxt1 translation is suppressed by Mir6996-3p. Considering previous reports and our current results we propose a model for Pxt1 regulation in the mouse male germ cells.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.theriogenology.2023.07.010 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mouse Pxt1 expression is regulated by Mir6996 miRNA.
Theriogenology
October 2023
Department of Genetics and Evolution, Institute of Zoology and Biomedical Research, Jagiellonian University, Gronostajowa 9, 30-387, Krakow, Poland. Electronic address:
Mouse Pxt1 gene is expressed exclusively in male germ cells and encodes for a small, cell death inducing protein. However, upon PXT1 interaction with BAG6, cell death is prevented. In transiently transfected cell lines the PXT1 expression triggered massive cell death, thus we ask the question whether the interaction of PXT1 and BAG6 is the only mechanism preventing normal, developing male germ cells from being killed by PXT1.
View Article and Find Full Text PDFIncreased DNA strand breaks in spermatozoa of knockout mice.
Reprod Fertil Dev
July 2023
Laboratory of Genetics and Evolutionism, Institute of Zoology and Biomedical Research, Jagiellonian University in Kraków, Kraków, Poland.
Context: The Pxt1 gene encodes a male germ cell-specific protein and its overexpression results in male germ cell degeneration and male infertility in transgenic mice.
Aims: The analysis of the function of Pxt1 during mouse spermatogenesis.
Methods: The phenotype of Pxt1 knockout mice was characterised by testicular histology, assessment of semen parameters including sperm motility, and DNA fragmentation by flow cytometry.
Structural basis for proapoptotic activation of Bak by the noncanonical BH3-only protein Pxt1.
PLoS Biol
June 2023
Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.
Article Synopsis
- Bak is a key player in apoptosis, part of the Bcl-2 family, and activates through binding with specific proapoptotic proteins.
- The study focused on how Pxt1, a protein found only in the testis, interacts with Bak, leading to Bak's activation and promoting cell death.
- By determining the crystal structure of the Bak-Pxt1 complex, researchers discovered that Pxt1 is a novel activator of Bak, enhancing our understanding of apoptosis signaling pathways.
Structural Analysis of the Interaction between Bcl-xL and the Noncanonical BH3 Domain of Non-Bcl-2 Family Proteins.
Curr Protein Pept Sci
June 2023
Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea.
Anti-apoptotic and anti-autophagic Bcl-2 homologues commonly contain a hydrophobic groove in which the BH3 domain is accommodated. The BH3 domain is usually considered a feature of Bcl-2 family members; however, it has also been found in various non-Bcl-2 family proteins. Although interactions among Bcl-2 family members have been extensively investigated and highlighted, those mediated by the BH3 domain of non-Bcl-2 family proteins have not been the focus of substantial research.
View Article and Find Full Text PDFPeptides from human BNIP5 and PXT1 and non-native binders of pro-apoptotic BAK can directly activate or inhibit BAK-mediated membrane permeabilization.
Structure
March 2023
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA. Electronic address:
Article Synopsis
- Apoptosis is crucial for proper development and maintaining tissue balance, and its disruption can lead to diseases like cancer.
- BAK, an apoptotic effector, changes shape to disrupt mitochondria and trigger cell death, with activation induced by human peptides like BID, BIM, and PUMA.
- Researchers identified ten new peptides that also activate BAK, providing insights into the complexity of peptide interactions that could lead to potential therapeutic tools targeting BAK.
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!