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Supplemental Material for Milano et al., 2019

dataset
posted on 03.04.2019, 14:52 by Carolyn R. Milano, J. Kim Holloway, Yongwei Zhang, Bo Jin, Cameron Smith, Aviv Bergman, Winfried Edelmann, Paula E. Cohen
MSH4/MSH5 are critical components of the class I crossover (CO) machinery, which is responsible for >90% of the COs that arise in mammalian meiosis. We generated a point mutation in the ATP binding motif of Msh5, and found that mutant spermatocytes lose all COs, not just those arising from the class I pathway.

History

Article title

Mutation of the ATPase Domain of MutS Homolog-5 (MSH5) Reveals a Requirement for a Functional MutSγ Complex for All Crossovers in Mammalian Meiosis

Manuscript #

G3/2019/400074R1

Article DOI

10.1534/g3.119.400074

Licence

Exports