NLRP14 Safeguards Calcium Homeostasis via Regulating the K27 Ubiquitination of Nclx in Oocyte‐to‐Embryo Transition

Sperm‐induced Ca 2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca 2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca 2+ oscillations and early embryonic dev...

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Published inAdvanced science Vol. 10; no. 27; pp. e2301940 - n/a
Main Authors Meng, Tie‐Gang, Guo, Jia‐Ni, Zhu, Liu, Yin, Yike, Wang, Feng, Han, Zhi‐Ming, Lei, Lei, Ma, Xue‐Shan, Xue, Yue, Yue, Wei, Nie, Xiao‐Qing, Zhao, Zheng‐Hui, Zhang, Hong‐Yong, Sun, Si‐Min, Ouyang, Ying‐Chun, Hou, Yi, Schatten, Heide, Ju, Zhenyu, Ou, Xiang‐Hong, Wang, Zhen‐Bo, Wong, Catherine C. L., Li, Zhonghan, Sun, Qing‐Yuan
Format Journal Article
LanguageEnglish
Published Germany John Wiley & Sons, Inc 01.09.2023
John Wiley and Sons Inc
Wiley
Subjects
adenosine triphosphate (ATP)
calcium homeostasis
CRISPR
DNA methylation
early embryonic development
Embryos
Females
Genes
Homeostasis
Infertility
Localization
maternal effect genes
Mitochondria
Mutation
NCLX
Ovaries
Ovulation
Proteins
Sperm
Uterus
NLRP14
maternal effect genes
early embryonic development
NCLX
UHRF1
adenosine triphosphate (ATP)
mitochondria
calcium homeostasis
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Abstract Sperm‐induced Ca 2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca 2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca 2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2‐cell stage. The impaired developmental potential of Nlrp14 ‐deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14 ‐deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin‐like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14 ‐deficient oocytes, and Uhrf1 ‐deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na + /Ca 2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14 mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27‐linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.
AbstractList Sperm-induced Ca2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2-cell stage. The impaired developmental potential of Nlrp14-deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14-deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14-deficient oocytes, and Uhrf1-deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na+/Ca2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27-linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.
Abstract Sperm‐induced Ca2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2‐cell stage. The impaired developmental potential of Nlrp14‐deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14‐deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin‐like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14‐deficient oocytes, and Uhrf1‐deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na+/Ca2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27‐linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.
Sperm‐induced Ca 2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca 2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca 2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2‐cell stage. The impaired developmental potential of Nlrp14 ‐deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14 ‐deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin‐like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14 ‐deficient oocytes, and Uhrf1 ‐deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na + /Ca 2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14 mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27‐linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.
Sperm‐induced Ca 2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca 2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca 2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2‐cell stage. The impaired developmental potential of Nlrp14 ‐deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14 ‐deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin‐like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14 ‐deficient oocytes, and Uhrf1 ‐deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na + /Ca 2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14 mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27‐linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development. The authors show that calcium homeostasis including Ca 2+ concentration dynamics, mitochondria dynamics, and ATP level are affected in Nlrp14 ‐deficient oocytes as well as in Uhrf1 ‐deficient oocytes during oocyte‐to‐embryo transition. Moreover, they demonstrate that NLRP14 interacts with the NCLX IDRs domain and maintains its stability by regulating the K27‐linked ubiquitination.
Sperm-induced Ca2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2-cell stage. The impaired developmental potential of Nlrp14-deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14-deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14-deficient oocytes, and Uhrf1-deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na+ /Ca2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27-linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.Sperm-induced Ca2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca2+ oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca2+ oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2-cell stage. The impaired developmental potential of Nlrp14-deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14-deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14-deficient oocytes, and Uhrf1-deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na+ /Ca2+ exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14mNull oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27-linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.
Sperm-induced Ca rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca oscillations are regulated. Here it is shown that NLRP14, a maternal effect factor, is essential for keeping Ca oscillations and early embryonic development. Few embryos lacking maternal NLRP14 can develop beyond the 2-cell stage. The impaired developmental potential of Nlrp14-deficient oocytes is mainly caused by disrupted cytoplasmic function and calcium homeostasis due to altered mitochondrial distribution, morphology, and activity since the calcium oscillations and development of Nlrp14-deficient oocytes can be rescued by substitution of whole cytoplasm by spindle transfer. Proteomics analysis reveal that cytoplasmic UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) is significantly decreased in Nlrp14-deficient oocytes, and Uhrf1-deficient oocytes also show disrupted calcium homeostasis and developmental arrest. Strikingly, it is found that the mitochondrial Na /Ca exchanger (NCLX) encoded by Slc8b1 is significantly decreased in the Nlrp14 oocyte. Mechanistically, NLRP14 interacts with the NCLX intrinsically disordered regions (IDRs) domain and maintain its stability by regulating the K27-linked ubiquitination. Thus, the study reveals NLRP14 as a crucial player in calcium homeostasis that is important for early embryonic development.
Author Nie, Xiao‐Qing
Han, Zhi‐Ming
Sun, Qing‐Yuan
Ma, Xue‐Shan
Guo, Jia‐Ni
Wong, Catherine C. L.
Schatten, Heide
Zhu, Liu
Yin, Yike
Yue, Wei
Ju, Zhenyu
Wang, Feng
Sun, Si‐Min
Meng, Tie‐Gang
Zhao, Zheng‐Hui
Ouyang, Ying‐Chun
Xue, Yue
Ou, Xiang‐Hong
Zhang, Hong‐Yong
Lei, Lei
Wang, Zhen‐Bo
Hou, Yi
Li, Zhonghan
AuthorAffiliation 7 Key Laboratory of Regenerative Medicine of Ministry of Education Institute of Aging and Regenerative Medicine Jinan University Guangzhou Guangdong 510632 P. R. China
2 State Key Laboratory of Stem Cell and Reproductive Biology Institute of Zoology Chinese Academy of Sciences Beijing 100101 P. R. China
8 Department of Medical Research Center State Key Laboratory of Complex Severe and Rare Diseases Peking Union Medical College Hospital Chinese Academy of Medical Science & Peking Union Medical College Beijing 100730 P. R. China
1 Fertility Preservation Lab Guangdong‐Hong Kong Metabolism and Reproduction Joint Laboratory Reproductive Medicine Center Guangdong Second Provincial General Hospital Guangzhou 510317 P. R. China
3 School of Basic Medical Sciences Peking University Health Science Center Beijing 100191 P. R. China
5 Department of Histology and Embryology Harbin Medical University Harbin 150088 P. R. China
9 Tsinghua University‐Peking University Joint Center for Life Sciences Tsinghua U
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/37493331$$D View this record in MEDLINE/PubMed
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Issue 27
Keywords NLRP14
maternal effect genes
early embryonic development
NCLX
UHRF1
adenosine triphosphate (ATP)
mitochondria
calcium homeostasis
Language English
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Snippet Sperm‐induced Ca 2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca 2+...
Sperm-induced Ca rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca oscillations are...
Sperm-induced Ca2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca2+ oscillations...
Abstract Sperm‐induced Ca2+ rise is critical for driving oocyte activation and subsequent embryonic development, but little is known about how lasting Ca2+...
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SubjectTerms adenosine triphosphate (ATP)
calcium homeostasis
CRISPR
DNA methylation
early embryonic development
Embryos
Females
Genes
Homeostasis
Infertility
Localization
maternal effect genes
Mitochondria
Mutation
NCLX
Ovaries
Ovulation
Proteins
Sperm
Uterus
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Title NLRP14 Safeguards Calcium Homeostasis via Regulating the K27 Ubiquitination of Nclx in Oocyte‐to‐Embryo Transition
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