Genes to Cells最新文献_第7页

Identification of Gallbladder-Specific Distal Regulatory Sequence of Murine Sox17 小鼠胆囊特异性Sox17远端调控序列的鉴定。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-12-26 DOI: 10.1111/gtc.13186

Shihan Zeng, Ayaka Yanagida, Noriaki Ota, Mami Uemura, Yoshikazu Hirate, Ryuji Hiramatsu, Naoaki Mizuno, Yoshiakira Kanai, Masami Kanai-Azuma

{"title":"Identification of Gallbladder-Specific Distal Regulatory Sequence of Murine Sox17","authors":"Shihan Zeng, Ayaka Yanagida, Noriaki Ota, Mami Uemura, Yoshikazu Hirate, Ryuji Hiramatsu, Naoaki Mizuno, Yoshiakira Kanai, Masami Kanai-Azuma","doi":"10.1111/gtc.13186","DOIUrl":"10.1111/gtc.13186","url":null,"abstract":"Sox17 is a key transcriptional regulator of endoderm formation and function in the gallbladder, blood vessels and reproductive organs. Although multiple transcript variants of Sox17 have been suggested, the precise mechanisms underlying their time- and tissue-specific expression remain unclear. In this study, we discovered two putative regulatory sequences (R1 and R2) adjacent to different transcription start sites of mouse Sox17 exon 1 and generated deletion mice for these regions (Sox17Δdr/Δdr). Sox17Δdr/Δdr mice were alive and fertile, and they possessed a normal-sized gallbladder. However, semiquantitative analysis of immunostaining showed that the expression levels of SOX17 in Sox17Δdr/Δdr embryos were reduced to less than 50% of the wild-type in the gallbladder epithelium. Furthermore, the bile ductal epithelium marker SOX9 was abnormally upregulated, and PAS/DBA-positive mucin secretion-like epithelial cells were induced in the Sox17Δdr/Δdr gallbladder. Our results demonstrate that the distal sequence of Sox17, including R1 and R2, is important for the regulation of Sox17 gene expression in the embryonic gallbladder and is crucial for normal gallbladder epithelial development.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894066","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

Interferon-Dependent Expression of the Human STAT1 Gene Requires a Distal Regulatory Region Located Approximately 6 kb Upstream for Its Autoregulatory System 人类STAT1基因的干扰素依赖性表达需要一个位于上游约6kb的远端调控区来实现其自动调控系统。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-12-25 DOI: 10.1111/gtc.13188

Katsutoshi Yuasa, Aimi Masubuchi, Tomo Okada, Miho Shinya, Yui Inomata, Honoka Kida, Sayoko Shyouji, Hirona Ichikawa, Tetsuyuki Takahashi, Masashi Muroi, Takao Hijikata

{"title":"Interferon-Dependent Expression of the Human STAT1 Gene Requires a Distal Regulatory Region Located Approximately 6 kb Upstream for Its Autoregulatory System","authors":"Katsutoshi Yuasa, Aimi Masubuchi, Tomo Okada, Miho Shinya, Yui Inomata, Honoka Kida, Sayoko Shyouji, Hirona Ichikawa, Tetsuyuki Takahashi, Masashi Muroi, Takao Hijikata","doi":"10.1111/gtc.13188","DOIUrl":"10.1111/gtc.13188","url":null,"abstract":"<div>\u0000 \u0000 We previously suggested that the signal transducer and activator of transcription 1 (STAT1) gene is autoregulated in an interferon (IFN)-dependent manner via a distal regulatory region approximately 5.5–6.2 kb upstream of the murine and human STAT1 promoters (designated 5.5URR). Here, we examined whether this IFN-dependent positive feedback mechanism of the STAT1 gene actually functions in cells. First, we created human embryonic kidney 293 cell mutants lacking the IFN-responsive transcription factor binding sites (IFN-stimulated response element and IFN-gamma-activated sequence) within the 5.5URR and stimulated them with IFN-α/γ. The mutants showed a loss of response to IFN, indicating that the 5.5URR is essential for IFN-induced transcriptional enhancement in STAT1 gene expression. Second, we cloned the full-length 11 kb human STAT1 promoter, including the region upstream of the 5.5URR, from the start codon and linked it to a luciferase gene. Reporter assays showed that IFN-α/γ significantly activated the STAT1 promoter via the 5.5URR. Furthermore, recombinant DNA linking the full-length STAT1 promoter to STAT1 cDNA was introduced into STAT1-deficient cells. In vitro reconstitution experiments showed that IFN-α/γ stimulation increased STAT1 protein levels via the 5.5URR. These results demonstrate that the 5.5URR confers IFN-dependent autoregulation of the STAT1 promoter.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894068","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

Rapamycin Abrogates Aggregation of Human α-Synuclein Expressed in Fission Yeast via an Autophagy-Independent Mechanism 雷帕霉素通过不依赖自噬的机制抑制分裂酵母中表达的人α-突触核蛋白的聚集。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-12-18 DOI: 10.1111/gtc.13185

Yoshitaka Sugimoto, Teruaki Takasaki, Ryuga Yamada, Ryo Kurosaki, Tomonari Yamane, Reiko Sugiura

{"title":"Rapamycin Abrogates Aggregation of Human α-Synuclein Expressed in Fission Yeast via an Autophagy-Independent Mechanism","authors":"Yoshitaka Sugimoto, Teruaki Takasaki, Ryuga Yamada, Ryo Kurosaki, Tomonari Yamane, Reiko Sugiura","doi":"10.1111/gtc.13185","DOIUrl":"10.1111/gtc.13185","url":null,"abstract":"<div>\u0000 \u0000 Aggregation of alpha-synuclein (α-Syn) is implicated in the pathogenesis of several neurodegenerative disorders, such as Parkinson's disease and Dementia with Lewy bodies, collectively termed synucleinopathies. Thus, tremendous efforts are being made to develop strategies to prevent or inhibit α-Syn aggregation. Here, we genetically engineered fission yeast to express human α-Syn C-terminally fused to green fluorescent protein (GFP) at low and high levels. α-Syn was localized at the cell tips and septa at low-level expression. At high-level expression, α-Syn was observed to form cytoplasmic aggregates. Notably, rapamycin, a natural product that allosterically inhibits the mammalian target of rapamycin (mTOR) by forming a complex with FKBP12, and Torin1, a synthetic mTOR inhibitor that blocks ATP binding to mTOR, markedly reduced the number of cells harboring α-Syn aggregates. These mTOR inhibitors abrogate α-Syn aggregation without affecting α-Syn expression levels. Rapamycin, but not Torin1, failed to reduce α-Syn aggregation in the deletion cells of fkh1+, encoding FKBP12, indicating the requirement of FKBP12 for rapamycin-mediated inhibition of α-Syn aggregation. Importantly, the effect of rapamycin was also observed in the cells lacking atg1+, a key regulator of autophagy. Collectively, rapamycin abrogates human α-Syn aggregation expressed in fission yeast via an autophagy-independent mechanism mediated by FKBP12.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853657","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

Defects in the H3t Gene Cause an Increase in Leydig Cells With Impaired Spermatogenesis in Mice H3t基因缺陷导致小鼠间质细胞增加，精子发生受损。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-12-03 DOI: 10.1111/gtc.13182

Qianmei Wu, Miho Ito, Takeru Fujii, Kaori Tanaka, Kohta Nakatani, Yoshihiro Izumi, Takeshi Bamba, Takashi Baba, Kazumitsu Maehara, Kosuke Tomimatsu, Tatsuya Takemoto, Yasuyuki Ohkawa, Akihito Harada

{"title":"Defects in the H3t Gene Cause an Increase in Leydig Cells With Impaired Spermatogenesis in Mice","authors":"Qianmei Wu, Miho Ito, Takeru Fujii, Kaori Tanaka, Kohta Nakatani, Yoshihiro Izumi, Takeshi Bamba, Takashi Baba, Kazumitsu Maehara, Kosuke Tomimatsu, Tatsuya Takemoto, Yasuyuki Ohkawa, Akihito Harada","doi":"10.1111/gtc.13182","DOIUrl":"10.1111/gtc.13182","url":null,"abstract":"Abnormalities in spermatogenesis, a fundamental component of male reproductive function, can cause male infertility. Somatic cells constituting the testis microenvironment are essential for controlling normal spermatogenesis. Although testicular somatic cells are thought to sense and respond to germ cells to ensure proper spermatogenesis, the details of this signaling mechanism are unknown. Here, we investigated somatic cell dynamics in testicular tissue lacking spermatogenesis using the mice with deletion of the testis-specific histone H3 variant gene H3t. Testicular tissue sections of H3tΔ/Δ mice exhibited an increased interstitial area compared with those of wild-type mice, which was primarily attributed to an increase in Leydig cell numbers. Furthermore, this increase in Leydig cells led to increased testosterone synthesis, which occurred alongside cellular senescence-associated β-galactosidase activity. These findings suggest that Leydig cells monitor the progress of spermatogenesis and possess a mechanism to promote functional germ cell formation.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13182","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768143","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

Presence of Gut Microbiota Worsens D-Galactosamine and Lipopolysaccharide-Induced Hepatic Injury in Mice 肠道菌群的存在加重了d -半乳糖胺和脂多糖诱导的小鼠肝损伤。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-12-03 DOI: 10.1111/gtc.13183

Kazuma Ohshima, Satoru Torii, Shigeomi Shimizu

{"title":"Presence of Gut Microbiota Worsens D-Galactosamine and Lipopolysaccharide-Induced Hepatic Injury in Mice","authors":"Kazuma Ohshima, Satoru Torii, Shigeomi Shimizu","doi":"10.1111/gtc.13183","DOIUrl":"10.1111/gtc.13183","url":null,"abstract":"<div>\u0000 \u0000 Acute liver failure is a serious, life-threatening disease. Although the gut microbiota has been considered to play a role in liver failure, the extent to which it is involved in the pathogenesis of this disease has not been fully elucidated to date. Therefore, we here analyzed the importance of the presence of intestinal microbiota in the pathogenesis of acute liver injury, using D-galactosamine (D-GalN)/lipopolysaccharide (LPS)-treated mice, which is a widely used experimental model of acute liver injury. First, administration of the antibiotic polymyxin B markedly alleviated liver injury. Liver injury was also reduced in germ-free mice, leading to the conclusion that the presence of intestinal microbiota aggravates D-GalN/LPS-induced liver injury. The amount of bacteria and LPS transferred from the gut to the blood was not increased by D-GalN/LPS, suggesting that the worsening of liver injury was not simply owing to the entry of bacteria into the circulation. In conclusion, acute liver injury in polymyxin B-pretreated or germ-free mice was ameliorated by modulation of the gut microbiota. Modification of the gut microbiota using polymyxin B may hence have the potential to alleviate acute liver injury in human patients.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768147","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

Image Analysis Characterizes Phenotypic Variation in the Growth of Mushroom-Forming Fungus Schizophyllum commune 图像分析揭示了形成蘑菇的真菌 Schizophyllum commune 生长过程中的表型差异。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-11-26 DOI: 10.1111/gtc.13181

Hiromi Matsumae, Megumi Sudo, Tadashi Imanishi, Tsuyoshi Hosoya

{"title":"Image Analysis Characterizes Phenotypic Variation in the Growth of Mushroom-Forming Fungus Schizophyllum commune","authors":"Hiromi Matsumae, Megumi Sudo, Tadashi Imanishi, Tsuyoshi Hosoya","doi":"10.1111/gtc.13181","DOIUrl":"10.1111/gtc.13181","url":null,"abstract":"<div>\u0000 \u0000 Schizophyllum commune, a common wood-decay mushroom known for its extremely high genetic variation and as a rare cause of human respiratory diseases, could be a promising model fungus contributing to both biology and medicine. To better understand its phenotypic variation, we developed an image analysis system that quantifies morphological and physiological traits of mycelial colonies in Petri dishes. This study evaluated growth of six wild and one clinical isolates of Japanese S. commune, subjected to different temperatures and glucose concentrations, including a condition mimicking the human respiratory environment. Our analysis revealed that combinations of two growth indices, area and whiteness, and profiling by clustering algorithms highlighted strain-specific responses. For example, the clinical isolate was the whitest under the respiratory-like condition. We also found that the growth rate was strongly determined by glucose concentration, while the effects of temperature on growth varied among the strains, suggesting that while glucose preference is common in this species, responses to temperature differ between strains. This system showed sufficient sensitivity to detect variation in mycelial growth. Our study provides a key to unraveling morphological and physiological traits behind the high polymorphisms in S. commune, including the ability to colonize the human respiratory tract.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716000","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

Generation of Monosomy 21q Human iPS Cells by CRISPR/Cas9-Mediated Interstitial Megabase Deletion 通过 CRISPR/Cas9 介导的间质巨碱基缺失法生成 21q 单体人 iPS 细胞。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-11-24 DOI: 10.1111/gtc.13184

Masaya Egawa, Narumi Uno, Rina Komazaki, Yusuke Ohkame, Kyotaro Yamazaki, Chihiro Yoshimatsu, Yuki Ishizu, Yusaku Okano, Hitomaru Miyamoto, Mitsuhiko Osaki, Teruhiko Suzuki, Kazuyoshi Hosomichi, Yasunori Aizawa, Yasuhiro Kazuki, Kazuma Tomizuka

{"title":"Generation of Monosomy 21q Human iPS Cells by CRISPR/Cas9-Mediated Interstitial Megabase Deletion","authors":"Masaya Egawa, Narumi Uno, Rina Komazaki, Yusuke Ohkame, Kyotaro Yamazaki, Chihiro Yoshimatsu, Yuki Ishizu, Yusaku Okano, Hitomaru Miyamoto, Mitsuhiko Osaki, Teruhiko Suzuki, Kazuyoshi Hosomichi, Yasunori Aizawa, Yasuhiro Kazuki, Kazuma Tomizuka","doi":"10.1111/gtc.13184","DOIUrl":"10.1111/gtc.13184","url":null,"abstract":"Missing an entire chromosome or chromosome arm in normal diploid cells has a deleterious impact on cell viability, which may contribute to the development of specific birth defects. Nevertheless, the effects of chromosome loss in human cells have remained unexplored due to the lack of suitable model systems. Here, we developed an efficient, selection-free approach to generate partial monosomy in human induced pluripotent stem cells (iPSCs). The introduction of Cas9 proteins and a pair of gRNAs induces over megabase-sized interstitial chromosomal deletions. Using human chromosome 21 (HSA21) as a model, partial monosomy 21q (PM21q) iPSC lines with deletions ranging from 4.5 to 27.9 Mb were isolated. A 33.6 Mb deletion, encompassing all protein-coding genes on 21q, was also achieved, establishing the first 21q monosomy human iPSC line. Transcriptome and proteome analyses revealed that the abundances of mRNA and protein encoded by the majority of genes in the monosomic regions are half of the diploid expression level, indicating an absence of dosage compensation. The ability to generate customized partial monosomy cell lines on an isogenic, karyotypically normal background should facilitate the gain of novel insights into the impact of chromosome loss on cellular fitness.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13184","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709921","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

Chromosomal rearrangements associated with SMC5/6 deficiency in DNA replication 与 DNA 复制中 SMC5/6 缺乏有关的染色体重排。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2024-11-14 DOI: 10.1111/gtc.13180

Yoshiharu Kusano, Yasuha Kinugasa, Satoshi Tashiro, Toru Hirota

{"title":"Chromosomal rearrangements associated with SMC5/6 deficiency in DNA replication","authors":"Yoshiharu Kusano, Yasuha Kinugasa, Satoshi Tashiro, Toru Hirota","doi":"10.1111/gtc.13180","DOIUrl":"10.1111/gtc.13180","url":null,"abstract":"Completion of DNA replication before chromosome segregation is essential for the stable maintenance of the genome. Under replication stress, DNA synthesis may persist beyond S phase, especially in genomic regions that are difficult to proceed with the replication processes. Incomplete replication in mitosis emerges as non-disjoined segment in mitotic chromosomes leading to anaphase bridges. The resulting chromosome rearrangements are not well characterized, however. Here, we report that incomplete replication due to SMC5/6 deficiency impairs sister chromatid disjunction at difficult-to-replicate regions, including common fragile sites. These non-disjoined regions manifest as cytologically defined symmetric gaps, causing anaphase bridges. These bridges break at the gaps, leading to telomere loss, micronucleation, and fragmentation. Subsequently, fusions between telomere-deficient chromosomes generate complex chromosomal rearrangements, including dicentric chromosomes, suggesting the occurrence of breakage-fusion-bridge cycle. Additionally, chromosomes in micronuclei were pulverized, indicative of chromothripsis. Our findings suggest that incomplete replication facilitates complex chromosomal rearrangements, which may contribute to genomic instability in human cancers.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 12","pages":"1251-1263"},"PeriodicalIF":1.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618665","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 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":"10.1111/gtc.13178","url":null,"abstract":"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.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 12","pages":"1111-1117"},"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

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

引用次数: 0