Genes to Cells最新文献

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The fly brain lands in Tokyo: A report on the 3rd Asia Pacific Drosophila Neurobiology Conference. 蝇脑登陆东京:第三届亚太果蝇神经生物学会议报告。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-05 DOI: 10.1111/gtc.13178
Gaurav Das, Olfat A Malak, Khushboo Sharma, Abdalla G Alia, Swetha Gopalakrishnan, Reshma V Menon, Hayato M Yamanouchi, Akinao Nose, Hokto Kazama, Adrian W Moore, Takashi Suzuki
{"title":"The fly brain lands in Tokyo: A report on the 3rd Asia Pacific Drosophila Neurobiology Conference.","authors":"Gaurav Das, Olfat A Malak, Khushboo Sharma, Abdalla G Alia, Swetha Gopalakrishnan, Reshma V Menon, Hayato M Yamanouchi, Akinao Nose, Hokto Kazama, Adrian W Moore, Takashi Suzuki","doi":"10.1111/gtc.13178","DOIUrl":"https://doi.org/10.1111/gtc.13178","url":null,"abstract":"<p><p>The third Asia Pacific Drosophila Neurobiology Conference (APDNC3) was held in the Wako Campus of RIKEN in Tokyo, Japan, from February 27th to March 1st, 2024. While APDNC2 was held in Taiwan in 2019, the global coronavirus pandemic enforced a long hiatus. Hence, APDNC3 was a much-anticipated meeting that attracted ~218 scientists from 18 different countries and regions, 154 from outside Japan. The meeting was divided into 13 scientific, 2 poster, and 3 career development sessions. Two plenary talks were delivered by Professor Daisuke Yamamoto, from NICT and Professor Claude Desplan from NYU. Thirty-seven other speakers were invited to give lectures. Eighty-six poster presenters were selected from submitted abstracts. Talks and posters described how neuronal circuits underlying specific behaviors were identified and how they developed. The presented work also demonstrated circuit-specific cellular and molecular mechanisms in health and disease. It was clear that technological advances, like molecular genetic tools for identifying, manipulating, and imaging individual neurons and the great granularity of the fly brain connectome, were significantly augmenting research. Overall, the meeting highlighted the remarkable biological insights that fly neurobiologists continue to provide.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582847","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
Dose-dependent effects of histone methyltransferase NSD2 on site-specific double-strand break repair. 组蛋白甲基转移酶 NSD2 对位点特异性双链断裂修复的剂量依赖性效应
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-01 Epub Date: 2024-09-08 DOI: 10.1111/gtc.13156
Koh Iwasaki, Akari Tojo, Haruka Kobayashi, Kai Shimizu, Yoshitaka Kamimura, Yasunori Horikoshi, Atsuhiko Fukuto, Jiying Sun, Manabu Yasui, Masamitsu Honma, Atsushi Okabe, Ryoji Fujiki, Nakako Izumi Nakajima, Atsushi Kaneda, Satoshi Tashiro, Akira Sassa, Kiyoe Ura
{"title":"Dose-dependent effects of histone methyltransferase NSD2 on site-specific double-strand break repair.","authors":"Koh Iwasaki, Akari Tojo, Haruka Kobayashi, Kai Shimizu, Yoshitaka Kamimura, Yasunori Horikoshi, Atsuhiko Fukuto, Jiying Sun, Manabu Yasui, Masamitsu Honma, Atsushi Okabe, Ryoji Fujiki, Nakako Izumi Nakajima, Atsushi Kaneda, Satoshi Tashiro, Akira Sassa, Kiyoe Ura","doi":"10.1111/gtc.13156","DOIUrl":"10.1111/gtc.13156","url":null,"abstract":"<p><p>Histone modifications are catalyzed and recognized by specific proteins to regulate dynamic DNA metabolism processes. NSD2 is a histone H3 lysine 36 (H3K36)-specific methyltransferase that is associated with both various transcription regulators and DNA repair factors. Specifically, it has been implicated in the repair of DNA double-strand breaks (DSBs); however, the role of NSD2 during DSB repair remains enigmatic. Here, we show that NSD2 does not accumulate at DSB sites and that it is not further mobilized by DSB formation. Using three different DSB repair reporter systems, which contained the endonuclease site in the active thymidine kinase gene (TK) locus, we demonstrated separate dose-dependent effects of NSD2 on homologous recombination (HR), canonical-non-homologous end joining (c-NHEJ), and non-canonical-NHEJ (non-c-NHEJ). Endogenous NSD2 has a role in repressing non-c-NHEJ, without affecting DSB repair efficiency by HR or total NHEJ. Furthermore, overexpression of NSD2 promotes c-NHEJ repair and suppresses HR repair. Therefore, we propose that NSD2 has functions in chromatin integrity at the active regions during DSB repair.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153750","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
Accelerated BDNF expression in visceral white adipose tissues following high-fat diet feeding in mice. 小鼠摄入高脂饮食后,内脏白色脂肪组织中 BDNF 的表达加速。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-01 Epub Date: 2024-09-15 DOI: 10.1111/gtc.13162
Kurumi Sakata, Mamoru Fukuchi
{"title":"Accelerated BDNF expression in visceral white adipose tissues following high-fat diet feeding in mice.","authors":"Kurumi Sakata, Mamoru Fukuchi","doi":"10.1111/gtc.13162","DOIUrl":"10.1111/gtc.13162","url":null,"abstract":"<p><p>Brain-derived neurotrophic factor (BDNF) is expressed in the white adipose tissues (WATs), and the expression increases during high-fat diet (HFD) feeding, implicating its role in obesity. Here, we focused on BDNF expression in epididymal WAT (eWAT), a visceral adipose tissue, in mice. During 2 weeks of HFD feeding, Bdnf mRNA expression in eWAT slightly increased, but a robust increase was observed after 8 weeks of HFD feeding. This upregulation of Bdnf mRNA was correlated with significant induction of hypoxia-inducible factor 1α (Hif1α) and platelet-derived growth factor subunit B (Pdgfb) mRNA in eWAT following 8 weeks of HFD feeding. Furthermore, the increased expression of the M1 macrophage markers was strongly correlated with the elevation of Bdnf mRNA in the eWAT. Notably, 8 weeks of HFD feeding significantly elevated Tnfα mRNA expression in eWAT, while no such induction was observed in inguinal WAT (iWAT). In contrast, the expression of Adipoq (adiponectin), implicated in improved insulin sensitivity and anti-inflammatory effects, was significantly upregulated in iWAT, but not in eWAT. Thus, our study may show the role of BDNF in eWAT in obesity models, potentially contributing to the pathological state of visceral adipose tissues.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142284368","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
Regular exercise suppresses steatosis-associated liver cancer development by degrading E2F1 and c-Myc via circadian gene upregulation. 通过昼夜节律基因上调降解E2F1和c-Myc,定期运动可抑制脂肪变性相关肝癌的发展。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-01 Epub Date: 2024-10-02 DOI: 10.1111/gtc.13161
Vu Thuong Huyen, Kanae Echizen, Ryota Yamagishi, Miho Kumagai, Yoshiki Nonaka, Takahiro Kodama, Tatsuya Ando, Megumu Yano, Naoki Takada, Masaki Takasugi, Fumitaka Kamachi, Naoko Ohtani
{"title":"Regular exercise suppresses steatosis-associated liver cancer development by degrading E2F1 and c-Myc via circadian gene upregulation.","authors":"Vu Thuong Huyen, Kanae Echizen, Ryota Yamagishi, Miho Kumagai, Yoshiki Nonaka, Takahiro Kodama, Tatsuya Ando, Megumu Yano, Naoki Takada, Masaki Takasugi, Fumitaka Kamachi, Naoko Ohtani","doi":"10.1111/gtc.13161","DOIUrl":"10.1111/gtc.13161","url":null,"abstract":"<p><p>Regular exercise is believed to suppress cancer progression. However, the precise molecular mechanisms by which exercise prevents cancer development remain unclear. In this study, using a steatosis-associated liver cancer mouse model, we found that regular exercise at a speed of 18 m/min for 20 min daily suppressed liver cancer development. To explore the underlying mechanisms, we examined the gene expression profiles in the livers of the exercise and non-exercise groups. The expressions of circadian genes, such as Per1 and Cry2, were upregulated in the exercise group. As circadian rhythm disruption is known to cause various diseases, including cancer, improving circadian rhythm through exercise could contribute to cancer prevention. We further found that the expression of a series of E2F1 and c-Myc target genes that directly affect the proliferation of cancer cells was downregulated in the exercise group. However, the expression of E2F1 and c-Myc was transcriptionally unchanged but degraded at the post-translational level by exercise. Cry2, which is regulated by the Skp1-Cul1-FBXL3 (SCF<sup>FBXL3</sup>) ubiquitin ligase complex by binding to FBXL3, can form a complex with E2F1 and c-Myc, which we think is the mechanism to degrade them. Our study revealed a previously unknown mechanism by which exercise prevents cancer development.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365047","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 repertoire of G-protein-coupled receptor variations in the Japanese population 54KJPN. 日本人口中 G 蛋白偶联受体变异的剧目 54KJPN.
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-01 Epub Date: 2024-09-23 DOI: 10.1111/gtc.13164
Tatsuya Ikuta, Riko Suzuki, Asuka Inoue
{"title":"The repertoire of G-protein-coupled receptor variations in the Japanese population 54KJPN.","authors":"Tatsuya Ikuta, Riko Suzuki, Asuka Inoue","doi":"10.1111/gtc.13164","DOIUrl":"10.1111/gtc.13164","url":null,"abstract":"<p><p>G-protein-coupled receptors (GPCRs) are the largest superfamily in the human genome and the major targets for the market drugs. Recent massive genomics studies revealed numerous natural variations in the general population. 54KJPN is the most extensive Japanese population genomics study, curating the whole genome sequences from about 54,000 individuals. Here, by analyzing 390 non-olfactory GPCR genes in the 54KJPN dataset, we annotated 25,443 missense single-nucleotide variations. Among them, we found 120 major variations that appear with an allele frequency greater than 0.5, including variations that occurred on posttranslational modification sites. Structural alignment of GPCRs using the generic numbering system in the GPCRdb reveals enrichment of alterations in the conserved arginine residue within the DRY motif, which contributes to downstream G-protein signaling. A comparison with the worldwide 1000 Genomes Project (1KGP) dataset found 23 variations that were present exclusively in the 54KJPN dataset. This study will be the basis for future pharmacogenomics studies for the Japanese population.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142284369","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
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 : 2024-11-01 Epub 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":"10.1111/gtc.13155","url":null,"abstract":"<p><p>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<sup>/-</sup>, BRCA1<sup>-/-</sup>, and RAD18<sup>-/-</sup> 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<sup>-/-</sup> 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.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555630/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meta-analysis of gonadal transcriptome provides novel insights into sex change mechanism across protogynous fishes. 性腺转录组的元分析为了解原雌性鱼类的性别变化机制提供了新的视角。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-01 Epub Date: 2024-09-29 DOI: 10.1111/gtc.13166
Ryo Nozu, Mitsutaka Kadota, Masaru Nakamura, Shigehiro Kuraku, Hidemasa Bono
{"title":"Meta-analysis of gonadal transcriptome provides novel insights into sex change mechanism across protogynous fishes.","authors":"Ryo Nozu, Mitsutaka Kadota, Masaru Nakamura, Shigehiro Kuraku, Hidemasa Bono","doi":"10.1111/gtc.13166","DOIUrl":"10.1111/gtc.13166","url":null,"abstract":"<p><p>Protogyny, being capable of changing from female to male during their lifetime, is prevalent in 20 families of teleosts but is believed to have evolved within specific evolutionary lineages. Therefore, shared regulatory factors governing the sex change process are expected to be conserved across protogynous fishes. However, a comprehensive understanding of this mechanism remains elusive. To identify these factors, we conducted a meta-analysis using gonadal transcriptome data from seven species. We curated data pairs of ovarian tissue and transitional gonad, and employed ratios of expression level as a unified criterion for differential expression, enabling a meta-analysis across species. Our approach revealed that classical sex change-related genes exhibited differential expression levels between the ovary and transitional gonads, consistent with previous reports. These results validate our methodology's robustness. Additionally, we identified novel genes not previously linked to gonadal sex change in fish. Notably, changes in the expression levels of acetoacetyl-CoA synthetase and apolipoprotein Eb, which are involved in cholesterol synthesis and transport, respectively, suggest that the levels of cholesterol, a precursor of steroid hormones crucial for sex change, are decreased upon sex change onset in the gonads. This implies a potential universal influence of cholesterol dynamics on gonadal transformation in protogyny.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345082","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
Evolution of the Cdk4/6-Cdkn2 system in invertebrates. 无脊椎动物中 Cdk4/6-Cdkn2 系统的进化。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-11-01 Epub Date: 2024-10-08 DOI: 10.1111/gtc.13165
Shiori Yuki, Shunsuke Sasaki, Yuta Yamamoto, Fumika Murakami, Kazumi Sakata, Isato Araki
{"title":"Evolution of the Cdk4/6-Cdkn2 system in invertebrates.","authors":"Shiori Yuki, Shunsuke Sasaki, Yuta Yamamoto, Fumika Murakami, Kazumi Sakata, Isato Araki","doi":"10.1111/gtc.13165","DOIUrl":"10.1111/gtc.13165","url":null,"abstract":"<p><p>The cell cycle is driven by cyclin-dependent kinases (Cdks). The decision whether the cell cycle proceeds is made during G1 phase, when Cdk4/6 functions. Cyclin-dependent kinase inhibitor 2 (Cdkn2) is a specific inhibitor of Cdk4/6, and their interaction depends on D84 in Cdkn2 and R24/31 in Cdk4/6. This knowledge is based mainly on studies in mammalian cells. Here, we comprehensively analyzed Cdk4/6 and Cdkn2 in invertebrates and found that Cdk4/6 was present in most of the investigated phyla, but the distribution of Cdkn2 was rather uneven among and within the phyla. The positive charge of R24/R31 in Cdk4/6 was conserved in all analyzed species in phyla with Cdkn2. The presence of Cdkn2 and the conservation of the positive charge were statistically correlated. We also found that Cdkn2 has been tightly linked to Fas associated factor 1 (Faf1) during evolution. We discuss potential interactions between Cdkn2 and Cdk4/6 in evolution and the possible cause of the strong conservation of the microsynteny.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142389827","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
Immunotherapy-induced reprogramming of cancer-associated fibroblasts can promote tumor progression. 免疫疗法诱导的癌症相关成纤维细胞重编程可促进肿瘤进展。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-10-30 DOI: 10.1111/gtc.13177
Tomoya Yamashita, Haruki Horiguchi, Tsuyoshi Kadomatsu, Michio Sato, Toshiro Moroishi, Yuichi Oike
{"title":"Immunotherapy-induced reprogramming of cancer-associated fibroblasts can promote tumor progression.","authors":"Tomoya Yamashita, Haruki Horiguchi, Tsuyoshi Kadomatsu, Michio Sato, Toshiro Moroishi, Yuichi Oike","doi":"10.1111/gtc.13177","DOIUrl":"https://doi.org/10.1111/gtc.13177","url":null,"abstract":"<p><p>Use of immune checkpoint inhibitors (ICIs) as cancer immunotherapy has advanced rapidly in the clinic; however, ICI initiation can also cause an unexpectedly rapid acceleration of cancer progression in some patients. Here, we used a murine syngeneic melanoma model to conduct mechanistic analysis of cancer-associated fibroblast (CAF) function in cancer progression in the context of immunotherapy. We found that after ICI treatment CAFs acquire inflammatory properties, which can promote tumor progression. Mechanistically, we show that T-cell-derived interferon-γ (IFN-γ) stimulates production of tumor necrosis factor-α (TNF-α) by macrophages, facilitating CAF conversion to inflammatory CAFs. Our findings suggest that CAF/immune cell crosstalk plays an essential role in ICI-associated tumor progression.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545061","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
Mrc1Claspin is essential for heterochromatin maintenance in Schizosaccharomyces pombe. Mrc1Claspin对小鼠异染色质的维持至关重要。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2024-10-29 DOI: 10.1111/gtc.13175
Kei Kawakami, Yukari Ueno, Nao Hayama, Katsunori Tanaka
{"title":"Mrc1<sup>Claspin</sup> is essential for heterochromatin maintenance in Schizosaccharomyces pombe.","authors":"Kei Kawakami, Yukari Ueno, Nao Hayama, Katsunori Tanaka","doi":"10.1111/gtc.13175","DOIUrl":"https://doi.org/10.1111/gtc.13175","url":null,"abstract":"<p><p>In eukaryotes, maintenance of heterochromatin structure that represses gene expression during cell proliferation is essential for guaranteeing cell identity. However, how heterochromatin is maintained and transmitted to the daughter cells remains elusive. In this study, we constructed a reporter system to study the maintenance of heterochromatin in the subtelomeric region of the fission yeast, Schizosaccharomyces pombe. We demonstrated that once subtelomeric heterochromatin was established, it tended to be maintained as a metastable structure through cell proliferation. Using this system, we screened an S. pombe genome-wide gene deletion library for subtelomeric heterochromatin maintenance factors and identified 57 genes related to various cellular processes, in addition to well-characterized heterochromatin factors. We focused on Mrc1<sup>Claspin</sup>, a mediator of DNA replication checkpoint. We found that Mrc1 maintains heterochromatin structure not only at the subtelomeres but also at the pericentromeres and mating-type regions. Furthermore, we showed that Mrc1 is required for the localization of Snf2/Hdac-containing Repressor Complex (SHREC) and the maintenance of hypoacetylation state of histone H3K14. This study complements the recent discoveries that Mrc1 functions as a histone H3-H4 chaperone in heterochromatin maintenance.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545062","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
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