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Gene Review

Spo11  -  SPO11 meiotic protein covalently bound to...

Mus musculus

Synonyms: AI449549, Meiotic recombination protein SPO11
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High impact information on Spo11

  • Genes expressed before the Spo11 block are enriched on the X chromosome, whereas those expressed later in spermatogenesis are depleted [1].
  • We used Spo11(-/-) mice blocked in spermatogenesis early in meiosis to evaluate the temporal pattern of gene expression in sperm development [1].
  • Our results report direct molecular evidence for distinct CR and NCR pathways of DNA double-strand break (DSB) repair in mouse meiosis based on three observations: both CRs and NCRs require Spo11, NCR products have shorter conversion tracts than CRs, and only CRs require the MutL homolog Mlh1 [2].
  • Chromosome synapsis defects and sexually dimorphic meiotic progression in mice lacking Spo11 [3].
  • The absence of ATM caused defects in folliculogenesis that were similar to those in Dmc1 mutants and that could be suppressed by Spo11 mutation, implying that oocyte death in Atm-deficient animals is a response to defective DSB repair [4].

Biological context of Spo11


Anatomical context of Spo11

  • Remarkably, we discovered that Spo11 heterozygosity can rescue the prophase-I-arrest characteristic of ATM-deficient spermatocytes [5].
  • To investigate whether Spo11 is involved in these processes, we studied the T cell dependent immune response of Spo11-deficient (Spo11(-/-)) mice against the hapten nitrophenyl (NP) [7].
  • Recently, we showed that mouse Spo11 is induced in normal mu(+) B cells by class switch recombination (CSR) stimuli, by RT-PCR using primers based on the reported cDNA sequence of testis-derived Spo11 (test-Spo11) cDNA [8].


  1. The mouse X chromosome is enriched for sex-biased genes not subject to selection by meiotic sex chromosome inactivation. Khil, P.P., Smirnova, N.A., Romanienko, P.J., Camerini-Otero, R.D. Nat. Genet. (2004) [Pubmed]
  2. Crossover and noncrossover pathways in mouse meiosis. Guillon, H., Baudat, F., Grey, C., Liskay, R.M., de Massy, B. Mol. Cell (2005) [Pubmed]
  3. Chromosome synapsis defects and sexually dimorphic meiotic progression in mice lacking Spo11. Baudat, F., Manova, K., Yuen, J.P., Jasin, M., Keeney, S. Mol. Cell (2000) [Pubmed]
  4. Distinct DNA-damage-dependent and -independent responses drive the loss of oocytes in recombination-defective mouse mutants. Di Giacomo, M., Barchi, M., Baudat, F., Edelmann, W., Keeney, S., Jasin, M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  5. SPO11 is required for sex-body formation, and Spo11 heterozygosity rescues the prophase arrest of Atm-/- spermatocytes. Bellani, M.A., Romanienko, P.J., Cairatti, D.A., Camerini-Otero, R.D. J. Cell. Sci. (2005) [Pubmed]
  6. Surveillance of different recombination defects in mouse spermatocytes yields distinct responses despite elimination at an identical developmental stage. Barchi, M., Mahadevaiah, S., Di Giacomo, M., Baudat, F., de Rooij, D.G., Burgoyne, P.S., Jasin, M., Keeney, S. Mol. Cell. Biol. (2005) [Pubmed]
  7. Mice deficient for the type II topoisomerase-like DNA transesterase Spo11 show normal immunoglobulin somatic hypermutation and class switching. Klein, U., Esposito, G., Baudat, F., Keeney, S., Jasin, M. Eur. J. Immunol. (2002) [Pubmed]
  8. Class switch recombination signals induce lymphocyte-derived Spo11 expression and Spo11 antisense oligonucleotide inhibits class switching. Tokuyama, H., Tokuyama, Y. Cell. Immunol. (2001) [Pubmed]
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