RT Journal Article SR Electronic T1 Spindle asymmetry drives non-Mendelian chromosome segregation JF bioRxiv FD Cold Spring Harbor Laboratory SP 180869 DO 10.1101/180869 A1 Takashi Akera A1 Lukáš Chmátal A1 Emily Trimm A1 Karren Yang A1 Chanat Aonbangkhen A1 David M. Chenoweth A1 Carsten Janke A1 Richard M. Schultz A1 Michael A. Lampson YR 2017 UL http://biorxiv.org/content/early/2017/08/27/180869.abstract AB Genetic elements compete for transmission through meiosis, when haploid gametes are created from a diploid parent. Selfish elements can enhance their transmission through meiotic drive, in violation of Mendel’s Law of Segregation. In female meiosis, selfish elements drive by preferentially attaching to the egg side of the spindle, which implies some asymmetry between the two sides of the spindle, but molecular mechanisms underlying spindle asymmetry are unknown. Here we show that CDC42 signaling from the cell cortex regulates microtubule tyrosination to induce spindle asymmetry, and non-Mendelian segregation depends on this asymmetry. These signals depend on cortical polarization directed by chromosomes, which are positioned near the cortex to allow the asymmetric cell division. Thus, selfish meiotic drivers exploit the asymmetry inherent in female meiosis to bias their transmission.