YTHDF2-mediated regulations bifurcate BHPF-induced programmed cell deaths
N -methyladenosine (m A) is a critical regulator in the fate of RNA, but whether and how m A executes its functions in different tissues remains largely obscure. Here we report downregulation of a crucial m A reader, YTHDF2, leading to tissue-specific programmed cell deaths (PCDs) upon fluorene-9-bi...
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| creator | Lin, Jiebo Zhan, Guankai Liu, Jinfeng Maimaitiyiming, Yasen Deng, Zhiping Li, Baohua Su, Kunhui Chen, Jiafeng Sun, Siqi Zheng, Wanlin Yu, Xianghui He, Feng Cheng, Xiaodong Wang, Lingfang Shen, Bin Yao, Ziqin Yang, Xinquan Zhang, Jian He, Wentao Wu, Hengyu Naranmandura, Hua Chang, Kao-Jung Min, Junxia Ma, Jun Björklund, Mikael Xu, Peng-Fei Wang, Fudi Hsu, Chih-Hung |
| description | N
-methyladenosine (m
A) is a critical regulator in the fate of RNA, but whether and how m
A executes its functions in different tissues remains largely obscure. Here we report downregulation of a crucial m
A reader, YTHDF2, leading to tissue-specific programmed cell deaths (PCDs) upon fluorene-9-bisphenol (BHPF) exposure. Currently, Bisphenol A (BPA) substitutes are widely used in plastic manufacturing. Interrogating eight common BPA substitutes, we detected BHPF in 14% serum samples of pregnant participants. In a zebrafish model, BHPF caused tissue-specific PCDs triggering cardiac and vascular defects. Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m
A-
for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m
A-
decay for caudal vein plexus (CVP) apoptosis. The two distinct YTHDF2-mediated m
A regulations and context-dependent co-expression patterns of
and
contributed to YTHDF2-mediated tissue-specific PCDs, uncovering a new layer of PCD regulation. Since BHPF/YTHDF2-medaited PCD defects were also observed in mammals, BHPF exposure represents a potential health threat. |
| doi_str_mv | 10.1093/nsr/nwad227 |
| format | Article |
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-methyladenosine (m
A) is a critical regulator in the fate of RNA, but whether and how m
A executes its functions in different tissues remains largely obscure. Here we report downregulation of a crucial m
A reader, YTHDF2, leading to tissue-specific programmed cell deaths (PCDs) upon fluorene-9-bisphenol (BHPF) exposure. Currently, Bisphenol A (BPA) substitutes are widely used in plastic manufacturing. Interrogating eight common BPA substitutes, we detected BHPF in 14% serum samples of pregnant participants. In a zebrafish model, BHPF caused tissue-specific PCDs triggering cardiac and vascular defects. Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m
A-
for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m
A-
decay for caudal vein plexus (CVP) apoptosis. The two distinct YTHDF2-mediated m
A regulations and context-dependent co-expression patterns of
and
contributed to YTHDF2-mediated tissue-specific PCDs, uncovering a new layer of PCD regulation. Since BHPF/YTHDF2-medaited PCD defects were also observed in mammals, BHPF exposure represents a potential health threat.</description><identifier>ISSN: 2095-5138</identifier><identifier>EISSN: 2053-714X</identifier><identifier>DOI: 10.1093/nsr/nwad227</identifier><identifier>PMID: 38152479</identifier><language>eng</language><publisher>China: Oxford University Press</publisher><ispartof>National science review, 2023-12, Vol.10 (12), p.nwad227-nwad227</ispartof><rights>The Author(s) 2023. Published by Oxford University Press on behalf of China Science Publishing & Media Ltd.</rights><rights>The Author(s) 2023. Published by Oxford University Press on behalf of China Science Publishing & Media Ltd. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c382t-aa5caa1e44cefb48954afebf0e0f5084b63f7904703585f966670a5fb97d44533</citedby><cites>FETCH-LOGICAL-c382t-aa5caa1e44cefb48954afebf0e0f5084b63f7904703585f966670a5fb97d44533</cites><orcidid>0000-0002-1990-4857 ; 0000-0001-8071-0122 ; 0000-0001-9663-3088 ; 0000-0001-8099-6327 ; 0000-0002-1609-3294 ; 0000-0001-8730-0003</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10751878/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10751878/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38152479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Jiebo</creatorcontrib><creatorcontrib>Zhan, Guankai</creatorcontrib><creatorcontrib>Liu, Jinfeng</creatorcontrib><creatorcontrib>Maimaitiyiming, Yasen</creatorcontrib><creatorcontrib>Deng, Zhiping</creatorcontrib><creatorcontrib>Li, Baohua</creatorcontrib><creatorcontrib>Su, Kunhui</creatorcontrib><creatorcontrib>Chen, Jiafeng</creatorcontrib><creatorcontrib>Sun, Siqi</creatorcontrib><creatorcontrib>Zheng, Wanlin</creatorcontrib><creatorcontrib>Yu, Xianghui</creatorcontrib><creatorcontrib>He, Feng</creatorcontrib><creatorcontrib>Cheng, Xiaodong</creatorcontrib><creatorcontrib>Wang, Lingfang</creatorcontrib><creatorcontrib>Shen, Bin</creatorcontrib><creatorcontrib>Yao, Ziqin</creatorcontrib><creatorcontrib>Yang, Xinquan</creatorcontrib><creatorcontrib>Zhang, Jian</creatorcontrib><creatorcontrib>He, Wentao</creatorcontrib><creatorcontrib>Wu, Hengyu</creatorcontrib><creatorcontrib>Naranmandura, Hua</creatorcontrib><creatorcontrib>Chang, Kao-Jung</creatorcontrib><creatorcontrib>Min, Junxia</creatorcontrib><creatorcontrib>Ma, Jun</creatorcontrib><creatorcontrib>Björklund, Mikael</creatorcontrib><creatorcontrib>Xu, Peng-Fei</creatorcontrib><creatorcontrib>Wang, Fudi</creatorcontrib><creatorcontrib>Hsu, Chih-Hung</creatorcontrib><title>YTHDF2-mediated regulations bifurcate BHPF-induced programmed cell deaths</title><title>National science review</title><addtitle>Natl Sci Rev</addtitle><description>N
-methyladenosine (m
A) is a critical regulator in the fate of RNA, but whether and how m
A executes its functions in different tissues remains largely obscure. Here we report downregulation of a crucial m
A reader, YTHDF2, leading to tissue-specific programmed cell deaths (PCDs) upon fluorene-9-bisphenol (BHPF) exposure. Currently, Bisphenol A (BPA) substitutes are widely used in plastic manufacturing. Interrogating eight common BPA substitutes, we detected BHPF in 14% serum samples of pregnant participants. In a zebrafish model, BHPF caused tissue-specific PCDs triggering cardiac and vascular defects. Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m
A-
for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m
A-
decay for caudal vein plexus (CVP) apoptosis. The two distinct YTHDF2-mediated m
A regulations and context-dependent co-expression patterns of
and
contributed to YTHDF2-mediated tissue-specific PCDs, uncovering a new layer of PCD regulation. Since BHPF/YTHDF2-medaited PCD defects were also observed in mammals, BHPF exposure represents a potential health threat.</description><issn>2095-5138</issn><issn>2053-714X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpVkc1LwzAYxoMobsydvEuPgtTls0lOotO5wUAPE_QU0jbZIl07k1bxvzdjc-gpL3l_7_N-PACcI3iNoCSjOvhR_aVLjPkR6GPISMoRfT3expKlDBHRA8MQ3iGECDPOCT4FPSIQw5TLPpi9Lab3E5yuTel0a8rEm2VX6dY1dUhyZztfxO_kbvo8SV1ddkVENr5Zer2OJUlhqiopjW5X4QycWF0FM9y_A_AyeViMp-n86XE2vp2nBRG4TbVmhdbIUFoYm1MhGdXW5BYaaBkUNM-I5RJSDgkTzMosyzjUzOaSl5QyQgbgZqe76fI4QmHq1utKbbxba_-tGu3U_0ztVmrZfCoEOUOCi6hwuVfwzUdnQqvWLmw30bVpuqCwhBxJnuEsolc7tPBNCN7YQx8E1dYAFQ1QewMiffF3tAP7e27yAyLcgzo</recordid><startdate>20231201</startdate><enddate>20231201</enddate><creator>Lin, Jiebo</creator><creator>Zhan, Guankai</creator><creator>Liu, Jinfeng</creator><creator>Maimaitiyiming, Yasen</creator><creator>Deng, Zhiping</creator><creator>Li, Baohua</creator><creator>Su, Kunhui</creator><creator>Chen, Jiafeng</creator><creator>Sun, Siqi</creator><creator>Zheng, Wanlin</creator><creator>Yu, Xianghui</creator><creator>He, Feng</creator><creator>Cheng, Xiaodong</creator><creator>Wang, Lingfang</creator><creator>Shen, Bin</creator><creator>Yao, Ziqin</creator><creator>Yang, Xinquan</creator><creator>Zhang, Jian</creator><creator>He, Wentao</creator><creator>Wu, Hengyu</creator><creator>Naranmandura, Hua</creator><creator>Chang, Kao-Jung</creator><creator>Min, Junxia</creator><creator>Ma, Jun</creator><creator>Björklund, Mikael</creator><creator>Xu, Peng-Fei</creator><creator>Wang, Fudi</creator><creator>Hsu, Chih-Hung</creator><general>Oxford University Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1990-4857</orcidid><orcidid>https://orcid.org/0000-0001-8071-0122</orcidid><orcidid>https://orcid.org/0000-0001-9663-3088</orcidid><orcidid>https://orcid.org/0000-0001-8099-6327</orcidid><orcidid>https://orcid.org/0000-0002-1609-3294</orcidid><orcidid>https://orcid.org/0000-0001-8730-0003</orcidid></search><sort><creationdate>20231201</creationdate><title>YTHDF2-mediated regulations bifurcate BHPF-induced programmed cell deaths</title><author>Lin, Jiebo ; 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-methyladenosine (m
A) is a critical regulator in the fate of RNA, but whether and how m
A executes its functions in different tissues remains largely obscure. Here we report downregulation of a crucial m
A reader, YTHDF2, leading to tissue-specific programmed cell deaths (PCDs) upon fluorene-9-bisphenol (BHPF) exposure. Currently, Bisphenol A (BPA) substitutes are widely used in plastic manufacturing. Interrogating eight common BPA substitutes, we detected BHPF in 14% serum samples of pregnant participants. In a zebrafish model, BHPF caused tissue-specific PCDs triggering cardiac and vascular defects. Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m
A-
for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m
A-
decay for caudal vein plexus (CVP) apoptosis. The two distinct YTHDF2-mediated m
A regulations and context-dependent co-expression patterns of
and
contributed to YTHDF2-mediated tissue-specific PCDs, uncovering a new layer of PCD regulation. Since BHPF/YTHDF2-medaited PCD defects were also observed in mammals, BHPF exposure represents a potential health threat.</abstract><cop>China</cop><pub>Oxford University Press</pub><pmid>38152479</pmid><doi>10.1093/nsr/nwad227</doi><orcidid>https://orcid.org/0000-0002-1990-4857</orcidid><orcidid>https://orcid.org/0000-0001-8071-0122</orcidid><orcidid>https://orcid.org/0000-0001-9663-3088</orcidid><orcidid>https://orcid.org/0000-0001-8099-6327</orcidid><orcidid>https://orcid.org/0000-0002-1609-3294</orcidid><orcidid>https://orcid.org/0000-0001-8730-0003</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Oxford Journals Open Access Collection; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| title | YTHDF2-mediated regulations bifurcate BHPF-induced programmed cell deaths |
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