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CREM activator and repressor isoform expression in human male germ cells
Sonja Blöcher1, Ludger Fink, Rainer M Bohle
1Clinic for General, Thorax and Visceral Surgery, University of Giessen, Germany.
International Journal of Andrology
|July 29, 2005
Summary
The cAMP-responsive element modulator (CREM) gene is crucial for male fertility. This study identified a new CREM repressor and found both activator and repressor isoforms in germ cells, suggesting a regulatory balance potentially disrupted in infertility.
Area of Science:
- Reproductive Biology
- Molecular Endocrinology
- Spermatogenesis Research
Background:
- The cAMP-responsive element modulator (CREM) transcription factor is essential for male fertility, with its absence causing infertility in mice.
- Alternative splicing of the CREM gene produces functionally diverse activator and repressor proteins.
- Reduced CREM activators and aberrant transcripts are observed in infertile men.
Purpose of the Study:
- To investigate the expression of CREM transcripts, including novel leader exons theta1 and theta2, in patients with impaired spermatogenesis.
- To identify new CREM repressor isoforms, such as theta1-F-H.
- To determine the localization of CREM activator and repressor isoforms within specific germ cell types.
Main Methods:
- Analysis of CREM transcript expression using leader exons theta1 and theta2.
- Identification of novel CREM isoforms via RT-PCR.
- Single-cell microdissection of seminiferous epithelium followed by RT-PCR to localize CREM isoforms.
Main Results:
- A new putative CREM repressor, theta1-F-H, was identified in patients with impaired spermatogenesis.
- CREM activator and repressor isoforms were detected in all germ cell types (spermatogonia, spermatocytes, round and elongated spermatids), but not in Sertoli cells.
- Higher expression of CREM activators was observed in spermatocytes and round spermatids compared to spermatogonia and elongated spermatids.
Conclusions:
- CREM activator and repressor isoforms are present across various germ cell types, challenging previous assumptions.
- A fine-tuning mechanism between CREM isoforms in normal germ cells is suggested.
- This regulatory balance may be disrupted in cases of impaired spermatogenesis.