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2003 | 50 | 2 | 535-541

Article title

Expression of a constitutively active mutant of heat shock factor 1 under the control of testis-specific hst70 gene promoter in transgenic mice induces degeneration of seminiferous epithelium.

Content

Title variants

Languages of publication

EN

Abstracts

EN
Heat shock activates in somatic cells a set of genes encoding heat shock proteins which function as molecular chaperones. The basic mechanism by which these genes are activated is the interaction of the specific transcription factor HSF1 with a regulatory DNA sequence called heat shock element (HSE). In higher eukaryotes HSF1 is present in unstressed cells as inactive monomers which, in response to cellular stress, aggregate into transcriptionally competent homotrimers. In the present paper we showed that the expression of a transgene encoding mutated constitutively active HSF1 placed under the control of a spermatocyte-specific promoter derived from the hst70 gene severely affects spermatogenesis. We found the testes of transgenic mice to be significantly smaller than those of wild-type males and histological analysis showed massive degeneration of the seminiferous epithelium. The lumen of tubules was devoid of spermatids and spermatozoa and using the TUNEL method we demonstrated a high rate of spermatocyte apoptosis. The molecular mechanism by which constitutively active HSF1 arrests spermatogenesis is not known so far. One can assume that HSF1 can either induce or repress so far unknown target genes involved in germ cell apoptosis.

Year

Volume

50

Issue

2

Pages

535-541

Physical description

Dates

published
2003
received
2002-11-19
revised
2003-02-11
accepted
2003-05-21

Contributors

  • Department of Tumor Biology, Center of Oncology, Maria Skłodowska-Curie Memorial Institute, Gliwice, Poland
  • Department of Tumor Biology, Center of Oncology, Maria Skłodowska-Curie Memorial Institute, Gliwice, Poland
  • Institute of Biochemistry, NAS of Belarus, Grodno, Belarus
  • Department of Tumor Biology, Center of Oncology, Maria Skłodowska-Curie Memorial Institute, Gliwice, Poland
  • Department of Tumor Biology, Center of Oncology, Maria Skłodowska-Curie Memorial Institute, Gliwice, Poland
  • Department of Tumor Biology, Center of Oncology, Maria Skłodowska-Curie Memorial Institute, Gliwice, Poland
author
  • Department of Biochemistry and Molecular Biology, Yamaguchi University School of Medicine, Ube, Japan
  • Department of Tumor Biology, Center of Oncology, Maria Skłodowska-Curie Memorial Institute, Gliwice, Poland

References

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Document Type

Publication order reference

Identifiers

YADDA identifier

bwmeta1.element.bwnjournal-article-abpv50i2p535kz
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