Xinwen Zheng
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Xinwen Zheng has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Arp Schnittger
Department of Developmental Biology, Institute of Plant Science and Microbiology University of Hamburg Hamburg 22609 Germany
1 shared publication - Chenjiang You
College of Life Sciences, Guangdong Provincial Key Laboratory for the Development Biology and Environmental Adaptation of Agricultural Organisms, South China Agricultural University, Guangzhou, Guangdong, China
1 shared publication - Cong Wang
Guangdong Basic Research Center of Excellence for Precise Breeding of Future Crops, Guangdong Laboratory for Lingnan Modern Agriculture, Guangdong Provincial Key Laboratory of Protein Function and Regulation in Agricultural Organisms, Engineering Research Center of Southern Soybean, Ministry of Education, College of Life Sciences, South China Agricultural University , Guangzhou 510642
1 shared publication - Ji Qi
State Key Laboratory of Wetland Conservation and Restoration, National Observations and Research Station for Wetland Ecosystems of the Yangtze Estuary, Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering, and Institute of Eco-Chongming, School of Life Sciences, Fudan University , Shanghai 200438
1 shared publication Jinchao Li
State Key Laboratory of Genetics and Development of Complex Phenotypes, Institute of Plant Biology, School of Life Sciences, Fudan University, Shanghai 200433, China
1 shared publication- Jun Wang
State Key Laboratory of Genetics and Development of Complex Phenotypes, Institute of Plant Biology, School of Life Sciences, Fudan University, Shanghai 200433, China
1 shared publication
Latest Publications
- 16 October 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Advances
- Vol. 12 (42)
Suppression of meiotic double-strand break formation in somatic cells by DREAM factors TCX5/6 maintains genome stability
Meiotic recombination in reproductive cells is initiated by DNA double-strand breaks (DSBs) and requires the expression of meiosis-specific genes, yet how the transcription of those genes is regulated in either meiotic or somatic cells remains unclear. Here, using a representative meiosis-specific DMC1 gene promoter as a bait, we identified two DREAM factors TCX5 and TCX6 required for direct repression of DMC1 in somatic cells. Transcriptomic analyses show broad ectopic up-regulation of meiotic genes in tcx5/6 leaves . Consistently, tcx5/6 somatic cells form DSBs and exhibit hypersensitivity to DNA damage compared to wild type. Further genetic analyses reveal that SPO11-1 is dispensable for ectopic meiotic gene activation but essential for the DNA damage response in tcx5/6 somatic cells. Last, we demonstrated that TCX5/6 repress meiotic gene expression through H3K4me3 modification. This finding uncovers an unexpected mechanism for suppressing meiotic recombination in somatic cells, thus preventing genetic diversity and genome instability in organisms.
- 16 October 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Advances
- Vol. 12 (42)
Suppression of meiotic double-strand break formation in somatic cells by DREAM factors TCX5/6 maintains genome stability
Meiotic recombination in reproductive cells is initiated by DNA double-strand breaks (DSBs) and requires the expression of meiosis-specific genes, yet how the transcription of those genes is regulated in either meiotic or somatic cells remains unclear. Here, using a representative meiosis-specific DMC1 gene promoter as a bait, we identified two DREAM factors TCX5 and TCX6 required for direct repression of DMC1 in somatic cells. Transcriptomic analyses show broad ectopic up-regulation of meiotic genes in tcx5/6 leaves . Consistently, tcx5/6 somatic cells form DSBs and exhibit hypersensitivity to DNA damage compared to wild type. Further genetic analyses reveal that SPO11-1 is dispensable for ectopic meiotic gene activation but essential for the DNA damage response in tcx5/6 somatic cells. Last, we demonstrated that TCX5/6 repress meiotic gene expression through H3K4me3 modification. This finding uncovers an unexpected mechanism for suppressing meiotic recombination in somatic cells, thus preventing genetic diversity and genome instability in organisms.