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<p>Stress conditions elicit the formation of different kinds of stress granules (SGs). Although male germ cells are particularly sensitive to heat stress, the composition of heat-induced SGs in the testis remains poorly characterized. Here, we show that ATXN2 is a main component of heat-induced SGs in male germ cells and identify a unique population of ATXN2-positive SGs in leptotene and zygotene spermatocytes lacking classical SG markers. The terminal nucleotidyltransferase 5A (TENT5A) is a cytoplasmic poly(A) polymerase that extends the poly(A) tails of mRNAs. <i>Tent5a</i> mRNA expression increases when somatic and germ cells are exposed to 42 °C, but not upon exposure to other stressors. In vitro, TENT5A extends the poly(A) tail of <i>Atxn2</i> transcripts, stabilizing them while repressing their translation. In heat-stressed testes, TENT5A depletion increases ATXN2-positive granules and reduces apoptosis in late pachytene spermatocytes. Thus, enhanced stress resilience in <i>Tent5a</i>-depleted male germ cells preserves spermatogenesis and rescues fertility following heat exposure.</p>

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The TENT5A-ATXN2 axis modulates germline and somatic cell survival during heat stress

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月14日

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  • Ru-pin Alicia Chi,
  • Ankit Gupta,
  • Yin Li,
  • Marine Baptissart,
  • Dongwon Lee,
  • Brian N. Papas,
  • Marcos Morgan

摘要

Stress conditions elicit the formation of different kinds of stress granules (SGs). Although male germ cells are particularly sensitive to heat stress, the composition of heat-induced SGs in the testis remains poorly characterized. Here, we show that ATXN2 is a main component of heat-induced SGs in male germ cells and identify a unique population of ATXN2-positive SGs in leptotene and zygotene spermatocytes lacking classical SG markers. The terminal nucleotidyltransferase 5A (TENT5A) is a cytoplasmic poly(A) polymerase that extends the poly(A) tails of mRNAs. Tent5a mRNA expression increases when somatic and germ cells are exposed to 42 °C, but not upon exposure to other stressors. In vitro, TENT5A extends the poly(A) tail of Atxn2 transcripts, stabilizing them while repressing their translation. In heat-stressed testes, TENT5A depletion increases ATXN2-positive granules and reduces apoptosis in late pachytene spermatocytes. Thus, enhanced stress resilience in Tent5a-depleted male germ cells preserves spermatogenesis and rescues fertility following heat exposure.