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A dioxin sensitive gene, mammalian WAPL, is implicated in spermatogenesis
Masahiko Kuroda1, Kosuke Oikawa, Tetsuya Ohbayashi
1Department of Pathology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8402, Japan. kuroda@tokyo-med.ac.jp
FEBS Letters
|December 29, 2004
Summary
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an endocrine disruptor, targets the mouse WAPL gene. TCDD affects mWAPL expression differently in cells with and without the AhR receptor, impacting male reproductive health.
Area of Science:
- Endocrinology
- Toxicology
- Molecular Biology
Background:
- 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent endocrine disruptor known for diverse toxic effects.
- The human WAPL (hWAPL) gene's function and its role in endocrine disruption are not fully understood.
Purpose of the Study:
- To identify TCDD target genes involved in its toxic effects.
- To investigate the role of mammalian WAPL genes in spermatogenesis and TCDD-induced reproductive toxicity.
Main Methods:
- cDNA representational difference analysis was used to identify TCDD-responsive genes in mouse embryonic stem cells.
- Quantitative analysis of mWAPL mRNA expression in mouse embryonic fibroblast cells with varying AhR receptor status upon TCDD exposure.
- Immunofluorescence microscopy to determine mWAPL localization in testicular chromosomes.
Main Results:
- Mouse WAPL (mWAPL), a homolog of hWAPL, was identified as a TCDD target gene.
- TCDD exposure modulated mWAPL expression in a manner dependent on the aryl hydrocarbon receptor (AhR) status.
- mWAPL is highly expressed in testes, localizes to the synaptonemal complex, and its expression decreases in mouse testes after TCDD injection.
Conclusions:
- Mammalian WAPL genes (hWAPL and mWAPL) are likely involved in spermatogenesis.
- mWAPL may function as a target gene mediating the reproductive toxicity associated with TCDD exposure.