Abstract
In maize, there are 2 meiotic drive systems that target large heterochromatic knobs composed of tandem repeats known as knob180 and TR-1. The first meiotic drive haplotype, abnormal chromosome 10 (Ab10) confers strong meiotic drive (∼75% transmission as a heterozygote) and encodes 2 kinesins: KINDR, which associates with knob180 repeats, and TRKIN, which associates with TR-1 repeats. Prior data show that meiotic drive is conferred primarily by the KINDR/knob180 system while the TRKIN/TR-1 system seems to have little or no role, making it unclear why Trkin has been maintained in Ab10 haplotypes. The second meiotic drive haplotype, K10L2, confers a low level of meiotic drive (∼51-52%) and only encodes the TRKIN/TR-1 system. Here, we used long-read sequencing to assemble the K10L2 haplotype and showed that it has strong homology to an internal portion of the Ab10 haplotype. We also carried out CRISPR mutagenesis to test the role of Trkin on Ab10 and K10L2. The data indicate that the Trkin gene on Ab10 does not improve drive or fitness but instead has a weak deleterious effect when paired with a normal chromosome 10. The deleterious effect is more severe when Ab10 is paired with K10L2: in this context, functional Trkin on either chromosome nearly abolishes Ab10 drive. Mathematical modeling based on the empirical data suggests that Trkin is unlikely to persist on Ab10. We conclude that Trkin either confers an advantage to Ab10 in untested circumstances or that it is in the process of being purged from the Ab10 population.