Genes to Cells最新文献_第2页

RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir. 依赖于 RAD18 和 BRCA1 的途径可促进细胞对核苷类似物更昔洛韦的耐受性。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-22 DOI: 10.1111/gtc.13155

Tasnim Ahmad, Ryotaro Kawasumi, Kouji Hirota

{"title":"RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir.","authors":"Tasnim Ahmad, Ryotaro Kawasumi, Kouji Hirota","doi":"10.1111/gtc.13155","DOIUrl":"https://doi.org/10.1111/gtc.13155","url":null,"abstract":"Ganciclovir (GCV) is a clinically important drug as it is used to treat viral infections. GCV is incorporated into the DNA during replication, where it interferes with subsequent replication on GCV-incorporated templates. However, the effects of GCV on the host genome and the mechanisms underlying cellular tolerance to GCV remain unclear. In this study, we explored these mechanisms using a collection of mutant DT40 cells. We identified RAD17/-, BRCA1-/-, and RAD18-/- cells as highly GCV-sensitive. RAD17, a component of the alternative checkpoint-clamp loader RAD17-RFC, was required for the activation of the intra-S checkpoint following GCV treatment. BRCA1, a critical factor for promoting homologous recombination (HR), was required for suppressing DNA double-strand breaks (DSBs). Moreover, RAD18, an E3-ligase involved in DNA repair, was critical in suppressing the aberrant ligation of broken chromosomes caused by GCV. We found that BRCA1 suppresses DSBs through HR-mediated repair and template switching (TS)-mediated damage bypass. Moreover, the strong GCV sensitivity of BRCA1-/- cells was rescued by the loss of 53BP1, despite the only partial restoration in the sister chromatid exchange events which are hallmarks of HR. These results indicate that BRCA1 promotes cellular tolerance to GCV through two mechanisms, TS and HR-mediated repair.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reconstruction of artificial nuclei with nuclear import activity in living mouse oocytes. 在活体小鼠卵母细胞中重建具有核输入活性的人工核。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-14 DOI: 10.1111/gtc.13149

Nao Yonezawa, Tomoko Shindo, Haruka Oda, Hiroshi Kimura, Yasushi Hiraoka, Tokuko Haraguchi, Kazuo Yamagata

{"title":"Reconstruction of artificial nuclei with nuclear import activity in living mouse oocytes.","authors":"Nao Yonezawa, Tomoko Shindo, Haruka Oda, Hiroshi Kimura, Yasushi Hiraoka, Tokuko Haraguchi, Kazuo Yamagata","doi":"10.1111/gtc.13149","DOIUrl":"https://doi.org/10.1111/gtc.13149","url":null,"abstract":"In eukaryotes, DNA is housed within the cell nucleus. Molecules required for the formation of a nucleus have been identified using in vitro systems with frog egg extracts and in vivo imaging of somatic cells. However, little is known about the physicochemical factors and conditions required for nuclear formation in mouse oocytes. In this study, using a reconstitution approach with purified DNA, we aimed to determine factors, such as the amount and timing of DNA introduction, required for the formation of nuclei with nuclear transport activity in mouse oocytes. T4 phage DNA (~166 kbp) was microinjected into strontium-activated oocytes to evaluate the conditions appropriate for nuclear formation. Microinjection of 100-500 ng/μL of T4 DNA, but not 20 ng/μL, was sufficient for the formation of nucleus-like structures. Furthermore, microinjection of DNA during metaphase II to telophase II, but not during interphase, was sufficient. Electron and fluorescence microscopy showed that T4 DNA-induced nucleus-like structures had nuclear lamina and nuclear pore complex structures similar to those of natural nuclei, as well as nuclear import activity. These results suggest that exogenous DNA can form artificial nuclei with nuclear transport functions in mouse oocytes, regardless of the sequence or source of the DNA.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Megakaryocyte maturation involves activation of the adaptive unfolded protein response. 巨核细胞的成熟涉及激活适应性未折叠蛋白反应。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-13 DOI: 10.1111/gtc.13151

M Faiz, M L Kalev-Zylinska, C Dunstan-Harrison, D C Singleton, M P Hay, E C Ledgerwood

引用次数: 0

Meflin/ISLR is a marker of adipose stem and progenitor cells in mice and humans that suppresses white adipose tissue remodeling and fibrosis. Meflin/ISLR 是小鼠和人类脂肪干细胞和祖细胞的标记，可抑制白色脂肪组织重塑和纤维化。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-13 DOI: 10.1111/gtc.13154

Toshikazu Ishihara, Katsuhiro Kato, Kotaro Matsumoto, Miyako Tanaka, Akitoshi Hara, Yukihiro Shiraki, Hidenori Morisaki, Yuya Urano, Ryota Ando, Kisuke Ito, Shinji Mii, Nobutoshi Esaki, Kazuhiro Furuhashi, Mikito Takefuji, Takayoshi Suganami, Toyoaki Murohara, Atsushi Enomoto

{"title":"Meflin/ISLR is a marker of adipose stem and progenitor cells in mice and humans that suppresses white adipose tissue remodeling and fibrosis.","authors":"Toshikazu Ishihara, Katsuhiro Kato, Kotaro Matsumoto, Miyako Tanaka, Akitoshi Hara, Yukihiro Shiraki, Hidenori Morisaki, Yuya Urano, Ryota Ando, Kisuke Ito, Shinji Mii, Nobutoshi Esaki, Kazuhiro Furuhashi, Mikito Takefuji, Takayoshi Suganami, Toyoaki Murohara, Atsushi Enomoto","doi":"10.1111/gtc.13154","DOIUrl":"https://doi.org/10.1111/gtc.13154","url":null,"abstract":"Identifying specific markers of adipose stem and progenitor cells (ASPCs) in vivo is crucial for understanding the biology of white adipose tissues (WAT). PDGFRα-positive perivascular stromal cells represent the best candidates for ASPCs. This cell lineage differentiates into myofibroblasts that contribute to the impairment of WAT function. However, ASPC marker protein(s) that are functionally crucial for maintaining WAT homeostasis are unknown. We previously identified Meflin as a marker of mesenchymal stem cells (MSCs) in bone marrow and tissue-resident perivascular fibroblasts in various tissues. We also demonstrated that Meflin maintains the undifferentiated status of MSCs/fibroblasts. Here, we show that Meflin is expressed in WAT ASPCs. A lineage-tracing experiment showed that Meflin+ ASPCs proliferate in the WAT of obese mice induced by a high-fat diet (HFD), while some of them differentiate into myofibroblasts or mature adipocytes. Meflin knockout mice fed an HFD exhibited a significant fibrotic response as well as increases in adipocyte cell size and the number of crown-like structures in WAT, accompanied by impaired glucose tolerance. These data suggested that Meflin expressed by ASPCs may have a role in reducing disease progression associated with WAT dysfunction.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The NADPH oxidases DUOX1 and DUOX2 are sorted to the apical plasma membrane in epithelial cells via their respective maturation factors DUOXA1 and DUOXA2. NADPH 氧化酶 DUOX1 和 DUOX2 通过各自的成熟因子 DUOXA1 和 DUOXA2 被分拣到上皮细胞的顶端质膜。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-10 DOI: 10.1111/gtc.13153

Akira Kohda, Sachiko Kamakura, Junya Hayase, Hideki Sumimoto

{"title":"The NADPH oxidases DUOX1 and DUOX2 are sorted to the apical plasma membrane in epithelial cells via their respective maturation factors DUOXA1 and DUOXA2.","authors":"Akira Kohda, Sachiko Kamakura, Junya Hayase, Hideki Sumimoto","doi":"10.1111/gtc.13153","DOIUrl":"https://doi.org/10.1111/gtc.13153","url":null,"abstract":"The membrane-integrated NADPH oxidases DUOX1 and DUOX2 are recruited to the apical plasma membrane in epithelial cells to release hydrogen peroxide, thereby playing crucial roles in various functions such as thyroid hormone synthesis and host defense. However, it has remained unknown about the molecular mechanism for apical sorting of DUOX1 and DUOX2. Here we show that DUOX1 and DUOX2 are correctly sorted to the apical membrane via the membrane-spanning DUOX maturation proteins DUOXA1 and DUOXA2, respectively, when co-expressed in MDCK epithelial cells. Impairment of N-glycosylation of DUOXA1 results in mistargeting of DUOX1 to the basolateral membrane. Similar to DUOX1 complexed with the glycosylation-defective DUOXA1, the naturally non-glycosylated oxidase NOX5, which forms a homo-oligomer, is targeted basolaterally. On the other hand, a mutant DUOXA2 deficient in N-glycosylation is less stable than the wild-type protein but still capable of recruiting DUOX2 to the apical membrane, whereas DUOX2 is missorted to the basolateral membrane when paired with DUOXA1. These findings indicate that DUOXA2 is crucial but its N-glycosylation is dispensable for DUOX2 apical recruitment; instead, its C-terminal region seems to be involved. Thus, apical sorting of DUOX1 and DUOX2 is likely regulated in a distinct manner by their respective partners DUOXA1 and DUOXA2.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141912388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Female-specific mechanisms of meiotic initiation and progression in mammalian oocyte development. 哺乳动物卵母细胞发育过程中雌性特有的减数分裂启动和进展机制

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-09 DOI: 10.1111/gtc.13152

Ryuki Shimada, Kei-Ichiro Ishiguro

{"title":"Female-specific mechanisms of meiotic initiation and progression in mammalian oocyte development.","authors":"Ryuki Shimada, Kei-Ichiro Ishiguro","doi":"10.1111/gtc.13152","DOIUrl":"https://doi.org/10.1111/gtc.13152","url":null,"abstract":"Meiosis is regulated in sexually dimorphic manners in mammals. In females, the commitment to and entry into meiosis are coordinated with the developmental program of oocytes. Female germ cells initiate meiosis within a short time window during the fetal period and then undergo meiotic arrest until puberty. However, the genetic mechanisms underlying the orchestration of oocyte development and meiosis to maximize the reproductive lifespan of mammalian females remain largely elusive. While meiotic initiation is regulated by a sexually common mechanism, where meiosis initiator and Stimulated by Retinoic Acid Gene 8 (STRA8) activate the meiotic genes, the female-specific mode of meiotic initiation is mediated by the interaction between retinoblastoma (RB) and STRA8. This review highlights the female-specific mechanisms of meiotic initiation and meiotic prophase progression in the context of oocyte development. Furthermore, the downstream pathway of the RB-STRA8 interaction that may regulate meiotic arrest will be discussed in the context of oocyte development, highlighting a potential genetic link between the female-specific mode of meiotic entry and meiotic arrest.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lineage tracing using Wnt2b-2A-CreERT2 knock-in mice reveals the contributions of Wnt2b-expressing cells to novel subpopulations of mesothelial/epicardial cell lineages during mouse development. 利用 Wnt2b-2A-CreERT2 基因敲入小鼠进行系谱追踪，揭示了小鼠发育过程中 Wnt2b 表达细胞对间皮细胞/心包细胞系新亚群的贡献。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-08-07 DOI: 10.1111/gtc.13147

Masanori Takahashi, Takayuki Isagawa, Tatsuyuki Sato, Norihiko Takeda, Kiyoshi Kawakami

{"title":"Lineage tracing using Wnt2b-2A-CreERT2 knock-in mice reveals the contributions of Wnt2b-expressing cells to novel subpopulations of mesothelial/epicardial cell lineages during mouse development.","authors":"Masanori Takahashi, Takayuki Isagawa, Tatsuyuki Sato, Norihiko Takeda, Kiyoshi Kawakami","doi":"10.1111/gtc.13147","DOIUrl":"https://doi.org/10.1111/gtc.13147","url":null,"abstract":"Mesothelial and epicardial cells give rise to various types of mesenchymal cells via epithelial (mesothelial)-to-mesenchymal transition during development. However, the genes controlling the differentiation and diversification of mesothelial/epicardial cells remain unclear. Here, we examined Wnt2b expression in the embryonic mesothelium and epicardium and performed lineage tracing of Wnt2b-expressing cells by using novel Wnt2b-2A-CreERT2 knock-in and LacZ-reporter mice. Wnt2b was expressed in mesothelial cells covering visceral organs, but the expression was restricted in their subpopulations. Wnt2b-expressing cells labeled at embryonic day (E) 10.5 were distributed to the mesothelium and mesenchyme in the lungs, abdominal wall, stomach, and spleen in Wnt2b2A-CreERT2/+;R26RLacZ/+ mice at E13.0. Wnt2b was initially expressed in the proepicardial organ (PEO) at E9.5 and then in the epicardium after E10.0. Wnt2b-expressing PEO cells labeled at E9.5 differentiated into a small fraction of cardiac fibroblasts and preferentially localized at the left side of the postnatal heart. LacZ+ epicardium-derived cells labeled at E10.5 differentiated into a small fraction of fibroblasts and smooth muscle cells in the postnatal heart. Taken together, our results reveal novel subpopulations of PEO and mesothelial/epicardial cells that are distinguishable by Wnt2b expression and elucidate the unique contribution of Wnt2b-expressing PEO and epicardial cells to the postnatal heart.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aging-associated reduction of chromosomal histones in mammalian oocytes. 哺乳动物卵母细胞中与衰老相关的染色体组蛋白减少。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-23 DOI: 10.1111/gtc.13146

Masashi Mori, Manami Koshiguchi, Osamu Takenouchi, Mei A Mukose, Hinako M Takase, Tappei Mishina, Hailiang Mei, Miho Kihara, Takaya Abe, Azusa Inoue, Tomoya S Kitajima

{"title":"Aging-associated reduction of chromosomal histones in mammalian oocytes.","authors":"Masashi Mori, Manami Koshiguchi, Osamu Takenouchi, Mei A Mukose, Hinako M Takase, Tappei Mishina, Hailiang Mei, Miho Kihara, Takaya Abe, Azusa Inoue, Tomoya S Kitajima","doi":"10.1111/gtc.13146","DOIUrl":"https://doi.org/10.1111/gtc.13146","url":null,"abstract":"Mammalian oocytes undergo a long-term meiotic arrest that can last for almost the entire reproductive lifespan. This arrest occurs after DNA replication and is prolonged with age, which poses a challenge to oocytes in maintaining replication-dependent chromosomal proteins required for the completion of meiosis. In this study, we show that chromosomal histones are reduced with age in mouse oocytes. Both types of histone H3 variants, replication-dependent H3.1/H3.2 and replication-independent H3.3, decrease with age. Aging-associated histone reduction is associated with transcriptomic features that are caused by genetic depletion of histone H3.3. Neither the genetic reduction of chromosomal H3.1/H3.2 nor H3.3 accelerates the aging-associated increase in premature chromosome separation that causes meiotic segregation errors. We suggest that aging-associated reduction of chromosomal histones is linked to several transcriptomic abnormalities but does not significantly contribute to errors in meiotic chromosome segregation during the reproductive lifespan of mice.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The interaction between the import carrier Hikeshi and HSP70 is modulated by heat, facilitating the nuclear import of HSP70 under heat stress conditions 导入载体Hikeshi和HSP70之间的相互作用受热调节，在热胁迫条件下促进了HSP70的核导入。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-10 DOI: 10.1111/gtc.13145

Shingo Kose, Sakie Yoshioka, Yutaka Ogawa, Ai Watanabe, Naoko Imamoto

{"title":"The interaction between the import carrier Hikeshi and HSP70 is modulated by heat, facilitating the nuclear import of HSP70 under heat stress conditions","authors":"Shingo Kose, Sakie Yoshioka, Yutaka Ogawa, Ai Watanabe, Naoko Imamoto","doi":"10.1111/gtc.13145","DOIUrl":"10.1111/gtc.13145","url":null,"abstract":"Heat stress strongly triggers the nuclear localization of the molecular chaperone HSP70. Hikeshi functions as a unique nuclear import carrier of HSP70. However, how the nuclear import of HSP70 is activated in response to heat stress remains unclear. Here, we investigated the effects of heat on the nuclear import of HSP70. In vitro transport assays revealed that pretreatment of the test samples with heat facilitated the nuclear import of HSP70. Furthermore, binding of Hikeshi to HSP70 increased when temperatures rose. These results indicated that heat is one of the factors that activates the nuclear import of HSP70. Previous studies showed that the F97A mutation in Hikeshi in an extended loop induced an opening in the hydrophobic pocket and facilitated the translocation of Hikeshi through the nuclear pore complex. We found that nuclear accumulation of HSP70 occurred at a lower temperature in cells expressing the Hikeshi-F97A mutant than in cells expressing wild-type Hikeshi. Collectively, our results show that the movement of the extended loop may play an important role in the interaction of Hikeshi with both FG (phenylalanine-glycine)-nucleoporins and HSP70 in a temperature-dependent manner, resulting in the activation of nuclear import of HSP70 in response to heat stress.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141579496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Histone H3.3 chaperone HIRA renders stress-responsive genes poised for prospective lethal stresses in acquired tolerance 组蛋白 H3.3 合子 HIRA 使应激反应基因在获得性耐受中准备好应对未来的致命应激。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-08 DOI: 10.1111/gtc.13140

Yoshikazu Nagagaki, Yuji Kozakura, Theventhiran Mahandaran, Yukiko Fumoto, Ryuichiro Nakato, Katsuhiko Shirahige, Fuyuki Ishikawa

{"title":"Histone H3.3 chaperone HIRA renders stress-responsive genes poised for prospective lethal stresses in acquired tolerance","authors":"Yoshikazu Nagagaki, Yuji Kozakura, Theventhiran Mahandaran, Yukiko Fumoto, Ryuichiro Nakato, Katsuhiko Shirahige, Fuyuki Ishikawa","doi":"10.1111/gtc.13140","DOIUrl":"10.1111/gtc.13140","url":null,"abstract":"Appropriate responses to environmental challenges are imperative for the survival of all living organisms. Exposure to low-dose stresses is recognized to yield increased cellular fitness, a phenomenon termed hormesis. However, our molecular understanding of how cells respond to low-dose stress remains profoundly limited. Here we report that histone variant H3.3-specific chaperone, HIRA, is required for acquired tolerance, where low-dose heat stress exposure confers resistance to subsequent lethal heat stress. We found that human HIRA activates stress-responsive genes, including HSP70, by depositing histone H3.3 following low-dose stresses. These genes are also marked with histone H3 Lys-4 trimethylation and H3 Lys-9 acetylation, both active chromatin markers. Moreover, depletion of HIRA greatly diminished acquired tolerance, both in normal diploid fibroblasts and in HeLa cells. Collectively, our study revealed that HIRA is required for eliciting adaptive stress responses under environmental fluctuations and is a master regulator of stress tolerance.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0