Genes to Cells最新文献_第3页

Cryo-EM structure and biochemical analyses of the nucleosome containing the cancer-associated histone H3 mutation E97K 含有癌症相关组蛋白 H3 突变 E97K 的核小体的低温电子显微镜结构和生化分析。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-07 DOI: 10.1111/gtc.13143

Tomoaki Kimura, Seiya Hirai, Tomoya Kujirai, Risa Fujita, Mitsuo Ogasawara, Haruhiko Ehara, Shun-ichi Sekine, Yoshimasa Takizawa, Hitoshi Kurumizaka

{"title":"Cryo-EM structure and biochemical analyses of the nucleosome containing the cancer-associated histone H3 mutation E97K","authors":"Tomoaki Kimura, Seiya Hirai, Tomoya Kujirai, Risa Fujita, Mitsuo Ogasawara, Haruhiko Ehara, Shun-ichi Sekine, Yoshimasa Takizawa, Hitoshi Kurumizaka","doi":"10.1111/gtc.13143","DOIUrl":"10.1111/gtc.13143","url":null,"abstract":"The Lys mutation of the canonical histone H3.1 Glu97 residue (H3E97K) is found in cancer cells. Previous biochemical analyses revealed that the nucleosome containing the H3E97K mutation is extremely unstable as compared to the wild-type nucleosome. However, the mechanism by which the H3E97K mutation causes nucleosome instability has not been clarified yet. In the present study, the cryo-electron microscopy structure of the nucleosome containing the H3E97K mutation revealed that the entry/exit DNA regions of the H3E97K nucleosome are disordered, probably by detachment of the nucleosomal DNA from the H3 N-terminal regions. This may change the intra-molecular amino acid interactions with the replaced H3 Lys97 residue, inducing structural distortion around the mutated position in the nucleosome. Consistent with the nucleosomal DNA end flexibility and the nucleosome instability, the H3E97K mutation exhibited reduced binding of linker histone H1 to the nucleosome, defective activation of PRC2 (the essential methyltransferase for facultative heterochromatin formation) with a poly-nucleosome, and enhanced nucleosome transcription by RNA polymerase II.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13143","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554702","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

Fatty acid preference for beta-oxidation in mitochondria of murine cultured astrocytes 小鼠培养的星形胶质细胞线粒体中脂肪酸的β-氧化偏好。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-04 DOI: 10.1111/gtc.13144

Laarni Grace Corales, Hitoshi Inada, Yuji Owada, Noriko Osumi

引用次数: 0

Protein degradation by a component of the chaperonin-linked protease ClpP 伴侣蛋白连接蛋白酶 ClpP 的一种成分对蛋白质的降解作用。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-04 DOI: 10.1111/gtc.13141

Fumihiro Ishikawa, Michio Homma, Genzoh Tanabe, Takayuki Uchihashi

引用次数: 0

An N-terminal and ankyrin repeat domain interactome of Shank3 identifies the protein complex with the splicing regulator Nono in mice Shank3的N-末端和杏仁蛋白重复结构域相互作用组确定了与小鼠剪接调节因子Nono的蛋白质复合物。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-07-04 DOI: 10.1111/gtc.13142

Sayaka Okuzono, Fumihiko Fujii, Daiki Setoyama, Ryoji Taira, Yohei Shinmyo, Hiroki Kato, Keiji Masuda, Kousuke Yonemoto, Satoshi Akamine, Yuki Matsushita, Yoshitomo Motomura, Takeshi Sakurai, Hiroshi Kawasaki, Kihoon Han, Takahiro A. Kato, Hiroyuki Torisu, Dongchon Kang, Yusaku Nakabeppu, Shouichi Ohga, Yasunari Sakai

{"title":"An N-terminal and ankyrin repeat domain interactome of Shank3 identifies the protein complex with the splicing regulator Nono in mice","authors":"Sayaka Okuzono, Fumihiko Fujii, Daiki Setoyama, Ryoji Taira, Yohei Shinmyo, Hiroki Kato, Keiji Masuda, Kousuke Yonemoto, Satoshi Akamine, Yuki Matsushita, Yoshitomo Motomura, Takeshi Sakurai, Hiroshi Kawasaki, Kihoon Han, Takahiro A. Kato, Hiroyuki Torisu, Dongchon Kang, Yusaku Nakabeppu, Shouichi Ohga, Yasunari Sakai","doi":"10.1111/gtc.13142","DOIUrl":"10.1111/gtc.13142","url":null,"abstract":"An autism-associated gene Shank3 encodes multiple splicing isoforms, Shank3a-f. We have recently reported that Shank3a/b-knockout mice were more susceptible to kainic acid-induced seizures than wild-type mice at 4 weeks of age. Little is known, however, about how the N-terminal and ankyrin repeat domains (NT-Ank) of Shank3a/b regulate multiple molecular signals in the developing brain. To explore the functional roles of Shank3a/b, we performed a mass spectrometry-based proteomic search for proteins interacting with GFP-tagged NT-Ank. In this study, NT-Ank was predicted to form a variety of complexes with a total of 348 proteins, in which RNA-binding (n = 102), spliceosome (n = 22), and ribosome-associated molecules (n = 9) were significantly enriched. Among them, an X-linked intellectual disability-associated protein, Nono, was identified as a NT-Ank-binding protein. Coimmunoprecipitation assays validated the interaction of Shank3 with Nono in the mouse brain. In agreement with these data, the thalamus of Shank3a/b-knockout mice aberrantly expressed splicing isoforms of autism-associated genes, Nrxn1 and Eif4G1, before and after seizures with kainic acid treatment. These data indicate that Shank3 interacts with multiple RNA-binding proteins in the postnatal brain, thereby regulating the homeostatic expression of splicing isoforms for autism-associated genes after birth.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534213","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

The CRK14 gene encoding a cysteine-rich receptor-like kinase is implicated in the regulation of global proliferative arrest in Arabidopsis thaliana 编码富半胱氨酸受体样激酶的 CRK14 基因与拟南芥全球增殖停滞的调控有关。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-06-28 DOI: 10.1111/gtc.13139

Sho Imai, Hikaru Hirozawa, Shingo Sugahara, Chisato Ishizaki, Mayu Higuchi, Yuma Matsushita, Takamasa Suzuki, Nobuyoshi Mochizuki, Akira Nagatani, Chiharu Ueguchi

{"title":"The CRK14 gene encoding a cysteine-rich receptor-like kinase is implicated in the regulation of global proliferative arrest in Arabidopsis thaliana","authors":"Sho Imai, Hikaru Hirozawa, Shingo Sugahara, Chisato Ishizaki, Mayu Higuchi, Yuma Matsushita, Takamasa Suzuki, Nobuyoshi Mochizuki, Akira Nagatani, Chiharu Ueguchi","doi":"10.1111/gtc.13139","DOIUrl":"10.1111/gtc.13139","url":null,"abstract":"Global proliferative arrest (GPA) is a phenomenon in monocarpic plants in which the activity of all aboveground meristems generally ceases in a nearly coordinated manner after the formation of a certain number of fruits. Despite the fact that GPA is a biologically and agriculturally important event, the underlying molecular mechanisms are not well understood. In this study, we attempted to elucidate the molecular mechanism of GPA regulation by identifying the gene responsible for the Arabidopsis mutant fireworks (fiw), causing an early GPA phenotype. Map-based cloning revealed that the fiw gene encodes CYSTEIN-RICH RECEPTOR-LIKE KINASE 14 (CRK14). Genetic analysis suggested that fiw is a missense, gain-of-function allele of CRK14. Since overexpression of the extracellular domain of CRK14 resulted in delayed GPA in the wild-type background, we concluded that CRK14 is involved in GPA regulation. Analysis of double mutants revealed that fiw acts downstream of or independently of the FRUITFULL-APETALA2 (AP2)/AP2-like pathway, which was previously reported as an age-dependent default pathway in GPA regulation. In addition, fiw is epistatic to clv with respect to GPA control. Furthermore, we found a negative effect on WUSCHEL expression in the fiw mutants. These results thus suggest the existence of a novel CRK14-dependent signaling pathway involved in GPA regulation.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141467509","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

The hibernation promoting factor of Betaproteobacteria Comamonas testosteroni cannot induce 100S ribosome formation but stabilizes 70S ribosomal particles Betaproteobacteria Comamonas testosteroni 的冬眠促进因子不能诱导 100S 核糖体的形成，但能稳定 70S 核糖体颗粒。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-06-27 DOI: 10.1111/gtc.13137

Masami Ueta, Akira Wada, Chieko Wada

{"title":"The hibernation promoting factor of Betaproteobacteria Comamonas testosteroni cannot induce 100S ribosome formation but stabilizes 70S ribosomal particles","authors":"Masami Ueta, Akira Wada, Chieko Wada","doi":"10.1111/gtc.13137","DOIUrl":"10.1111/gtc.13137","url":null,"abstract":"Bacteria use several means to survive under stress conditions such as nutrient depletion. One such response is the formation of hibernating 100S ribosomes, which are translationally inactive 70S dimers. In Gammaproteobacteria (Enterobacterales), 100S ribosome formation requires ribosome modulation factor (RMF) and short hibernation promoting factor (HPF), whereas it is mediated by only long HPF in the majority of bacteria. Here, we investigated the role of HPFs of Comamonas testosteroni, which belongs to the Betaproteobacteria with common ancestor to the Gammaproteobacteria. C. testosteroni has two genes of HPF homologs of differing length (CtHPF-125 and CtHPF-119). CtHPF-125 was induced in the stationary phase, whereas CtHPF-119 conserved in many other Betaproteobacteria was not expressed in the culture conditions used here. Unlike short HPF and RMF, and long HPF, CtHPF-125 could not form 100S ribosome. We first constructed the deletion mutant of Cthpf-125 gene. When the deletion mutant grows in the stationary phase, 70S particles were degraded faster than in the wild strain. CtHPF-125 contributes to stabilizing the 70S ribosome. CtHPF-125 and CtHPF-119 both inhibited protein synthesis by transcription-translation in vitro. Our findings suggest that CtHPF-125 binds to ribosome, and stabilizes 70S ribosomes, inhibits translation without forming 100S ribosomes and supports prolonging life.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141467510","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

Mutational analysis of Mei5, a subunit of Mei5-Sae3 complex, in Dmc1-mediated recombination during yeast meiosis Mei5-Sae3复合体亚基Mei5在酵母减数分裂过程中Dmc1介导的重组中的突变分析

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-06-25 DOI: 10.1111/gtc.13138

Stephen Mwaniki, Priyanka Sawant, Osaretin P. Osemwenkhae, Yurika Fujita, Masaru Ito, Asako Furukohri, Akira Shinohara

引用次数: 0

Promoter characterization of relZ-bifunctional (pp)pGpp synthetase in mycobacteria 分枝杆菌中 relZ 双功能（pp）ppGpp 合成酶的启动子特征。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-06-24 DOI: 10.1111/gtc.13135

Neethu RS, Shubham Kumar Sinha, Sakshi Batra, Pavan Reddy Regatti, Kirtimaan Syal

{"title":"Promoter characterization of relZ-bifunctional (pp)pGpp synthetase in mycobacteria","authors":"Neethu RS, Shubham Kumar Sinha, Sakshi Batra, Pavan Reddy Regatti, Kirtimaan Syal","doi":"10.1111/gtc.13135","DOIUrl":"10.1111/gtc.13135","url":null,"abstract":"The second messenger guanosine 3',5'-bis(diphosphate)/guanosine tetraphosphate (ppGpp) and guanosine 3'-diphosphate 5'-triphosphate/guanosine pentaphosphate (pppGpp) ((p)ppGpp) has been shown to be crucial for the survival of mycobacteria under hostile conditions. Unexpectedly, deletion of primary (p)ppGpp synthetase-Rel did not completely diminish (p)ppGpp levels leading to the discovery of novel bifunctional enzyme-RelZ, which displayed guanosine 5'-monophosphate,3'-diphosphate (pGpp), ppGpp, and pppGpp ((pp)pGpp) synthesis and RNAseHII activity. What conditions does it express itself under, and does it work in concert with Rel? The regulation of its transcription and whether the Rel enzyme plays a role in such regulation remain unclear. In this article, we have studied relZ promoter and compared its activity with rel promoter in different growth conditions. We observed that the promoter activity of relZ was constitutive; it is weaker than rel promoter, lies within 200 bp upstream of translation-start site, and it increased under carbon starvation. Furthermore, the promoter activity of relZ was compromised in the rel-knockout strain in the stationary phase. Our study unveils the dynamic regulation of relZ promoter activity by SigA and SigB sigma factors in different growth phases in mycobacteria. Importantly, elucidating the regulatory network of RelZ would enable the development of the targeted interventions for treating mycobacterial infections.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141456321","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

A novel transcription factor Sdr1 involving sulfur depletion response in fission yeast 裂变酵母中涉及硫耗竭反应的新型转录因子 Sdr1

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-06-21 DOI: 10.1111/gtc.13136

Hokuto Ohtsuka, Kotaro Ohara, Takafumi Shimasaki, Yoshiko Hatta, Yasukichi Maekawa, Hirofumi Aiba

{"title":"A novel transcription factor Sdr1 involving sulfur depletion response in fission yeast","authors":"Hokuto Ohtsuka, Kotaro Ohara, Takafumi Shimasaki, Yoshiko Hatta, Yasukichi Maekawa, Hirofumi Aiba","doi":"10.1111/gtc.13136","DOIUrl":"10.1111/gtc.13136","url":null,"abstract":"In the fission yeast Schizosaccharomyces pombe, the response to sulfur depletion has been less studied compared to the response to nitrogen depletion. Our study reveals that the fission yeast gene, SPCC417.09c, plays a significant role in the sulfur depletion response. This gene encodes a protein with a Zn2Cys6 fungal-type DNA-binding domain and a transcription factor domain, and we have named it sdr1+ (sulfur depletion response 1). Interestingly, while sulfur depletion typically induces autophagy akin to nitrogen depletion, we found that autophagy was not induced under sulfur depletion in the absence of sdr1+. This suggests that sdr1+ is necessary for the induction of autophagy under conditions of sulfur depletion. Although sdr1+ is not essential for the growth of fission yeast, its overexpression, driven by the nmt1 promoter, inhibits growth. This implies that Sdr1 may possess cell growth-inhibitory capabilities. In addition, our analysis of Δsdr1 cells revealed that sdr1+ also plays a role in regulating the expression of genes associated with the phosphate depletion response. In conclusion, our study introduces Sdr1 as a novel transcription factor that contributes to an appropriate cellular nutrient starvation response. It does so by inhibiting inappropriate cell growth and inducing autophagy in response to sulfur depletion.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141520502","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

Antibiotic effects on gut microbiota modulate diet-induced metabolic dysfunction-associated steatohepatitis development in C57BL/6 mice 抗生素对肠道微生物群的影响可调节 C57BL/6 小鼠饮食诱导的代谢功能障碍相关性脂肪性肝炎的发展。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-06-12 DOI: 10.1111/gtc.13134

Shun Takano, Koudai Kani, Kaichi Kasai, Naoya Igarashi, Miyuna Kato, Kana Goto, Yudai Matsuura, Mayuko Ichimura-Shimizu, Shiro Watanabe, Koichi Tsuneyama, Yukihiro Furusawa, Yoshinori Nagai

{"title":"Antibiotic effects on gut microbiota modulate diet-induced metabolic dysfunction-associated steatohepatitis development in C57BL/6 mice","authors":"Shun Takano, Koudai Kani, Kaichi Kasai, Naoya Igarashi, Miyuna Kato, Kana Goto, Yudai Matsuura, Mayuko Ichimura-Shimizu, Shiro Watanabe, Koichi Tsuneyama, Yukihiro Furusawa, Yoshinori Nagai","doi":"10.1111/gtc.13134","DOIUrl":"10.1111/gtc.13134","url":null,"abstract":"The potential involvement of the gut microbiota in metabolic dysfunction-associated steatohepatitis (MASH) pathogenesis has garnered increasing attention. In this study, we elucidated the link between high-fat/cholesterol/cholate-based (iHFC)#2 diet-induced MASH progression and gut microbiota in C57BL/6 mice using antibiotic treatments. Treatment with vancomycin (VCM), which targets gram-positive bacteria, exacerbated the progression of liver damage, steatosis, and fibrosis in iHFC#2-fed C57BL/6 mice. The expression levels of inflammation- and fibrosis-related genes in the liver significantly increased after VCM treatment for 8 weeks. F4/80+ macrophage abundance increased in the livers of VCM-treated mice. These changes were rarely observed in the iHFC#2-fed C57BL/6 mice treated with metronidazole, which targets anaerobic bacteria. A16S rRNA sequence analysis revealed a significant decrease in α-diversity in VCM-treated mice compared with that in placebo-treated mice, with Bacteroidetes and Firmicutes significantly decreased, while Proteobacteria and Verrucomicrobia increased markedly. Finally, VCM treatment dramatically altered the level and balance of bile acid (BA) composition in iHFC#2-fed C57BL/6 mice. Thus, the VCM-mediated exacerbation of MASH progression depends on the interaction between the gut microbiota, BA metabolism, and inflammatory responses in the livers of iHFC#2-fed C57BL/6 mice.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141305835","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