ArticleEMBO reports2025
The E3 ubiquitin ligase adaptor KLHL8 targets ZAR1 to regulate maternal mRNA degradation in oocytes.
Huizhen Fan, Ruyi Liu, Ran Yu, Biaobang Chen, Qiaoli Li, Jian Mu, Weijie Wang, Tianyu Wu, Lin He, Lei Wang and 2 more
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In one paragraphArticle in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
Huizhen FanInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Ruyi LiuInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.ORCID 0000-0003-3863-3439 Ran YuInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Biaobang ChenNHC Key Lab of Reproduction Regulation (Shanghai Institute for Biomedical and Pharmaceutical Technologies), Fudan University, Shanghai, China.ORCID 0000-0002-9921-2155 Qiaoli LiInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Jian MuInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Weijie WangInternational Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, 200030, Shanghai, China.ORCID 0000-0002-5717-1818 Tianyu WuInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.ORCID 0000-0002-4295-7172 Lin HeBio-X Center, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, 200030, Shanghai, China.
Lei WangInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China. wangleiwanglei@fudan.edu.cn.ORCID 0000-0002-3400-0434 Qing SangInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China. sangqing@fudan.edu.cn.ORCID 0000-0002-9895-1394 Zhihua ZhangInstitute of Pediatrics, Children's Hospital of Fudan University, the Institutes of Biomedical Sciences, The State Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China. zhihuazhang_@fudan.edu.cn.ORCID 0000-0002-4725-883X Funding
MOST | National Key Research and Development Program of China (NKPs) 2021YFC2700100MOST | National Key Research and Development Program of China (NKPs) 2022YFC2702300MOST | National Key Research and Development Program of China (NKPs) 2024YFC2706600MOST | National Natural Science Foundation of China (NSFC) 32130029MOST | National Natural Science Foundation of China (NSFC) 82288102MOST | National Natural Science Foundation of China (NSFC) 82325021MOST | National Natural Science Foundation of China (NSFC) 82371662the Fund of Fudan University and Cao'ejiang Basic Research 24FCB01
6 · The paper itselfAbstract
Maternal protein homeostasis and timely degradation of maternal mRNAs are essential for meiotic cell-cycle progression and subsequent embryonic development, but the mechanisms of maternal protein degradation are poorly understood. Here, we show that KLHL8, a substrate adaptor of Cullin-RING E3 ubiquitin ligases, is highly expressed in mouse oocytes and co-localizes with mitochondria. Oocyte-specific deletion of Klhl8 causes oocyte maturation defects and female infertility. ZAR1, an RNA binding protein that is required for mitochondria-associated ribonucleoprotein domain (MARDO) dissolution, is specifically recognized and degraded by KLHL8-mediated ubiquitination. In Klhl8-deficient oocytes, ZAR1 accumulation causes abnormal MARDO and mitochondria clustering, correlating with impaired maternal mRNA decay. Supplementation with exogenous Klhl8 mRNA rescues the degradation of ZAR1 and the dissolution of the MARDO in Klhl8
Indexed as
Adaptor Proteins, Signal TransducingEgg ProteinsOocytesRNA-Binding ProteinsRNA, MessengerRNA, Messenger, StoredRNA StabilityUbiquitin-Protein LigasesAnimalsFemaleMiceMice, KnockoutMitochondriaProteolysisUbiquitinationAdaptor Proteins, Signal TransducingEgg ProteinsRNA-Binding ProteinsRNA, MessengerRNA, Messenger, StoredUbiquitin-Protein LigasesKLHL8Maternal mRNA DecayOocyte MaturationUbiquitinationZAR1
Identifiers
PMID40721554
PMCPMC12420792
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