Chromosome synapsis defects and sexually dimorphic meiotic progression in mice lacking Spo11.

By F. Baudat, K. Manova, J. P. Yuen, M. Jasin, Scott Keeney. Molecules and Cells, 2000

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Recombinational DNA double-strand breaks in mice precede synapsis (2001, background): “Consistent with a conserved role in mammalian meiosis, meiocytes in Spo11 −/− mice are either asynaptic or have limited (frequently non-homologous) synapsis; males also exhibit an early prophase arres”
Specific arrests of spermatogenesis in genetically modified and mutant mice (2004, background): “In male knock out mice, the pachytene stage is not reached and an abnormal zygotene dominates at which stage the cells arrest and enter apoptosis as confirmed histologically (Baudat et al., 2000; Romanienko and Camerini-Otero, 2000).”
Repair of strand breaks by homologous recombination. (2013, background): “SPO11, first identified as being defective in budding yeast sporulation (Esposito and Esposito 1969), which is the end product of successful meiosis, is homologous to the archael type VIA topoisomerase subunit with functional homologs identified in many eukaryotes (Keeney 2008), including mouse (Bau”
Meiotic Recombination: The Essence of Heredity. (2015, background): “2) (e.g., Baudat et al. 2000; Romanienko and Camerini-Otero 2000; Peoples et al. 2002; Tesse et al. 2003; Henderson and Keeney 2004; Zickler and Kleckner 2015).”