한빛사 논문
Divyashree C. Nageswaran1,3, Jaeil Kim2,3, Christophe Lambing1, Juhyun Kim2, Jihye Park2, Eun-Jung Kim2, Hyun Seob Cho2, Heejin Kim2, Dohwan Byun 2, Yeong Mi Park2, Pallas Kuo 1, Seungchul Lee2, Andrew J. Tock 1, Xiaohui Zhao 1, Ildoo Hwang 2, Kyuha Choi 1,2 ,* and Ian R. Henderson 1,*
1Department of Plant Sciences, University of Cambridge, Cambridge, UK.
2Department of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
3These authors contributed equally: Divyashree C. Nageswaran, Jaeil Kim
*Corresponding author
Abstract
Meiotic crossovers are tightly restricted in most eukaryotes, despite an excess of initiating DNA double-strand breaks. The majority of plant crossovers are dependent on class I interfering repair, with a minority formed via the class II pathway. Class II repair is limited by anti-recombination pathways; however, similar pathways repressing class I crossovers have not been identified. Here, we performed a forward genetic screen in Arabidopsis using fluorescent crossover reporters to identify mutants with increased or decreased recombination frequency. We identified HIGH CROSSOVER RATE1 (HCR1) as repressing crossovers and encoding PROTEIN PHOSPHATASE X1. Genome-wide analysis showed that hcr1 crossovers are increased in the distal chromosome arms. MLH1 foci significantly increase in hcr1 and crossover interference decreases, demonstrating an effect on class I repair. Consistently, yeast two-hybrid and in planta assays show interaction between HCR1 and class I proteins, including HEI10, PTD, MSH5 and MLH1. We propose that HCR1 plays a major role in opposition to pro-recombination kinases to restrict crossovers in Arabidopsis.
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