Histone Demethylase AMX-1 Regulates Fertility in a p53/CEP-1 Dependent Manner
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<jats:p>Histone methylation shapes the epigenetic configuration and adjusts multiple fundamental nuclear processes, including transcription, cell cycle control and DNA repair. The absence of histone demethylase LSD1/SPR-5 leads to progressive fertility defects as well as a reduction in brood size. Similarly, <jats:italic>C. elegans</jats:italic> LSD2 homolog AMX-1 has been implicated in regulating H3K4me2 and maintaining interstrand crosslinks (ICL) susceptibility. However, the mechanisms of how lack of AMX-1 induces sterility have not been addressed so far. This study investigated the histone demethylase AMX-1 in <jats:italic>C. elegans</jats:italic> and uncovered how <jats:italic>amx-1</jats:italic> contributes to sterility in a p53/CEP-1 dependent manner. We show that while sterility in <jats:italic>spr-5</jats:italic> mutants exhibited progressive over generations, <jats:italic>amx-1</jats:italic> mutants displayed non-transgenerational fertility defects. Also, <jats:italic>amx-1</jats:italic> mutants exhibited a reduced number of sperms and produced low brood size (LBS) or sterile worms that retain neither sperms nor germline nuclei, suggesting that fertility defects originated from germline development failure. Surprisingly, sterility exhibited in <jats:italic>amx-1</jats:italic> was mediated by p53/CEP-1 function. Consistent with this result, upregulation of Piwi expression in <jats:italic>amx-1</jats:italic> mutants suggested that AMX-1 is essential for germline development by regulating Piwi gene expressions. We propose that AMX-1 is required for proper Piwi expression and transposon silencing in a p53/CEP-1 dependent manner; thus, the absence of AMX-1 expression leads to defective meiotic development and sterility. This study elucidates how LSD2/AMX-1 contributes to sterility, therefore, expanding the boundaries of histone demethylase function.</jats:p>
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Ren, Xiaojing, Sisi Tian, Qinghao Meng and Hyun-Min Kim (n.d.). Histone Demethylase AMX-1 Regulates Fertility in a p53/CEP-1 Dependent Manner. Frontiers in Genetics, 13. 10.3389/fgene.2022.929716 Retrieved from https://hdl.handle.net/10161/25505.
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Hyun Min Kim
Hello, I am Hyun M. Kim, an Associate Professor at Duke Kunshan University, where I have been teaching and conducting research since 2022. My research focuses on the molecular mechanisms that maintain genome integrity and germline development, with particular interests in DNA damage repair and epigenetic regulation. I primarily use the model organism Caenorhabditis elegans to study how cells respond to genotoxic stress and how these responses are regulated throughout development.
I earned my Ph.D. in Applied Biology from the Georgia Institute of Technology and completed my postdoctoral training at Harvard Medical School, where I continued my research on DNA repair mechanisms. Prior to joining Duke Kunshan University, I served as an Associate Professor at Tianjin University, working in a highly international academic environment.
In my lab, we investigate the roles of histone demethylases (such as LSD-1 and AMX-1) and employ genome editing tools like CRISPR-Cas9 to study gene–environment interactions during germline development. We also explore how natural products and herbal extracts influence DNA repair pathways and fertility, in collaboration with Professor Borris’s lab.
As an educator, I strive to create a research environment that fosters curiosity, critical thinking, and collaboration. I support students in becoming independent thinkers who are not afraid to ask questions and pursue novel ideas. My lab welcomes students who are passionate about molecular genetics, genome biology, and developmental biology.
Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.