Next Article in Journal
PP2A Functions during Mitosis and Cytokinesis in Yeasts
Next Article in Special Issue
Helicase-Like Transcription Factor HLTF and E3 Ubiquitin Ligase SHPRH Confer DNA Damage Tolerance through Direct Interactions with Proliferating Cell Nuclear Antigen (PCNA)
Previous Article in Journal
Cryptotanshinone from the Salvia miltiorrhiza Bunge Attenuates Ethanol-Induced Liver Injury by Activation of AMPK/SIRT1 and Nrf2 Signaling Pathways
Previous Article in Special Issue
Are Leukaemic Stem Cells Restricted to a Single Cell Lineage?
Open AccessCommunication

PHLDA1 Does Not Contribute Directly to Heat Shock-Induced Apoptosis of Spermatocytes

Maria Sklodowska-Curie Institute–Oncology Center, Gliwice Branch, Wybrzeże Armii Krajowej 15, 44-101 Gliwice, Poland
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(1), 267;
Received: 29 November 2019 / Revised: 25 December 2019 / Accepted: 27 December 2019 / Published: 30 December 2019
(This article belongs to the Collection Feature Papers in Molecular Biology)
Spermatocytes are among the most heat-sensitive cells and the exposure of testes to heat shock results in their Heat Shock Factor 1 (HSF1)-mediated apoptosis. Several lines of evidence suggest that pleckstrin-homology-like domain family A, member 1 (PHLDA1) plays a role in promoting heat shock-induced cell death in spermatogenic cells, yet its precise physiological role is not well understood. Aiming to elucidate the hypothetical role of PHLDA1 in HSF1-mediated apoptosis of spermatogenic cells we characterized its expression in mouse testes during normal development and after heat shock. We stated that transcription of Phlda1 is upregulated by heat shock in many adult mouse organs including the testes. Analyzes of the Phlda1 expression during postnatal development indicate that it is expressed in pre-meiotic or somatic cells of the testis. It starts to be transcribed much earlier than spermatocytes are fully developed and its transcripts and protein products do not accumulate further in the later stages. Moreover, neither heat shock nor expression of constitutively active HSF1 results in the accumulation of PHLDA1 protein in meiotic and post-meiotic cells although both conditions induce massive apoptosis of spermatocytes. Furthermore, the overexpression of PHLDA1 in NIH3T3 cells leads to cell detachment, yet classical apoptosis is not observed. Therefore, our findings indicate that PHLDA1 cannot directly contribute to the heat-induced apoptosis of spermatocytes. Instead, PHLDA1 could hypothetically participate in death of spermatocytes indirectly via activation of changes in the somatic or pre-meiotic cells present in the testes. View Full-Text
Keywords: apoptosis; detachment; heat shock; HSF1; PHLDA1; spermatogenesis apoptosis; detachment; heat shock; HSF1; PHLDA1; spermatogenesis
Show Figures

Figure 1

MDPI and ACS Style

Janus, P.; Mrowiec, K.; Vydra, N.; Widłak, P.; Toma-Jonik, A.; Korfanty, J.; Smolarczyk, R.; Widłak, W. PHLDA1 Does Not Contribute Directly to Heat Shock-Induced Apoptosis of Spermatocytes. Int. J. Mol. Sci. 2020, 21, 267.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Search more from Scilit
Back to TopTop