Functional compensation for the loss of testis-specific poly(A)-binding protein, PABPC2, during mouse spermatogenesis

  • KASHIWABARA Shin-ichi
    Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan
  • TSURUTA Satsuki
    Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan
  • OKADA Keitaro
    Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan
  • SAEGUSA Ayaka
    Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan
  • MIYAGAKI Yu
    Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan
  • BABA Tadashi
    Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan Life Science Center of Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Ibaraki 305-8577, Japan

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Mouse testes contain several isoforms of cytoplasmic poly(A)-binding proteins (PABPCs), including ubiquitous PABPC1 and testis-specific PABPC2/PABPt. PABPC2 is characterized by its absence from translationally active polyribosomes and elongating spermatids. To elucidate the function of PABPC2 in spermatogenesis, we produced mutant mice lacking PABPC2. The PABPC2-null mice showed normal fertility. The processes of spermatogenesis and sperm migration in the testes and epididymides, respectively, were normal in the mutant mice. When the involvement of PABPC2 in translational regulation of haploid-specific mRNAs was examined, these mRNAs were correctly transcribed in round spermatids and translated in elongating spermatids. Moreover, immunoblot analysis revealed low abundance of PABPC2 relative to PABPC1 in spermatogenic cells. These results suggest that PABPC2 may be either functionally redundant with other PABPCs (including PABPC1) or largely dispensable for translational regulation during spermiogenesis.

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