Defects in recombination can preclude homologous chromosome pairing, leave unrepaired chromosome breaks, and cause aneuploidy by abrogating crossing over. To avoid such deleterious outcomes, surveillance systems (“checkpoints”) exist to sense meiotic errors and eliminate cells containing unresolved defects. In many organisms, including S. cerevisiae, Drosophila melanogaster, C. elegans, and mice [1–4], meiocytes with defects in recombination and/or chromosome synapsis trigger meiotic arrest in the pachytene stage of meiotic prophase I. This response to meiotic defects is referred to as the “pachytene checkpoint” (reviewed in [5]). Genetic experiments in S. cerevisiae have identified elements of the pachytene checkpoint machinery (reviewed in [5]). In addition to meiosis-specific proteins, these include factors that play roles in DNA damage signaling in mitotic cells [6–10]. Arabidopsis thaliana does not appear to have a pachytene checkpoint akin to that in yeast [11], nor do male Drosophila.