{"title":"竹荪 tpc2 基因缺失会形成多尖端结构，调节自噬和细胞类型模式化。","authors":"Madhubala Rathore, Ashima Thakur, Shweta Saran","doi":"10.1111/boc.202300067","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background Information</h3>\n \n <p>Two pore channels (TPCs) are voltage-gated ion channel superfamily members that release Ca<sup>2+</sup> from acidic intracellular stores and are ubiquitously present in both animals and plants. Starvation initiates multicellular development in <i>Dictyostelium discoideum</i>. Increased intracellular calcium levels bias <i>Dictyostelium</i> cells towards the stalk pathway and thus we decided to analyze the role of TPC2 in development, differentiation, and autophagy.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>We showed TPC2 protein localizes in lysosome-like acidic vesicles and the in situ data showed stalk cell biasness. Deletion of <i>tpc2</i> showed defective and delayed development with formation of multi-tipped structures attached to a common base, while <i>tpc2<sup>OE</sup></i> cells showed faster development with numerous small-sized aggregates and wiry fruiting bodies. The <i>tpc2<sup>OE</sup></i> cells showed higher intracellular cAMP levels as compared to the <i>tpc2<sup>−</sup></i> cells while pinocytosis was found to be higher in the <i>tpc2<sup>−</sup></i> cells. Also, TPC2 regulates cell-substrate adhesion and cellular morphology. Under nutrient starvation, deletion of <i>tpc2</i> reduced autophagic flux as compared to Ax2. During chimera formation, <i>tpc2<sup>−</sup></i> cells showed a bias towards the prestalk/stalk region while <i>tpc2<sup>OE</sup></i> cells showed a bias towards the prespore/spore region. <i>tpc2</i> deficient strain exhibits aberrant cell-type patterning and loss of distinct boundary between the prestalk/prespore regions.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>TPC2 is required for effective development and differentiation in <i>Dictyostelium</i> and supports autophagic cell death and cell-type patterning.</p>\n </section>\n \n <section>\n \n <h3> Significance</h3>\n \n <p>Decreased calcium due to deletion of <i>tpc2</i> inhibit autophagic flux.</p>\n </section>\n </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":null,"pages":null},"PeriodicalIF":2.4000,"publicationDate":"2024-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Deletion of Dictyostelium tpc2 gene forms multi-tipped structures, regulates autophagy and cell-type patterning\",\"authors\":\"Madhubala Rathore, Ashima Thakur, Shweta Saran\",\"doi\":\"10.1111/boc.202300067\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background Information</h3>\\n \\n <p>Two pore channels (TPCs) are voltage-gated ion channel superfamily members that release Ca<sup>2+</sup> from acidic intracellular stores and are ubiquitously present in both animals and plants. Starvation initiates multicellular development in <i>Dictyostelium discoideum</i>. Increased intracellular calcium levels bias <i>Dictyostelium</i> cells towards the stalk pathway and thus we decided to analyze the role of TPC2 in development, differentiation, and autophagy.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>We showed TPC2 protein localizes in lysosome-like acidic vesicles and the in situ data showed stalk cell biasness. Deletion of <i>tpc2</i> showed defective and delayed development with formation of multi-tipped structures attached to a common base, while <i>tpc2<sup>OE</sup></i> cells showed faster development with numerous small-sized aggregates and wiry fruiting bodies. The <i>tpc2<sup>OE</sup></i> cells showed higher intracellular cAMP levels as compared to the <i>tpc2<sup>−</sup></i> cells while pinocytosis was found to be higher in the <i>tpc2<sup>−</sup></i> cells. Also, TPC2 regulates cell-substrate adhesion and cellular morphology. Under nutrient starvation, deletion of <i>tpc2</i> reduced autophagic flux as compared to Ax2. During chimera formation, <i>tpc2<sup>−</sup></i> cells showed a bias towards the prestalk/stalk region while <i>tpc2<sup>OE</sup></i> cells showed a bias towards the prespore/spore region. <i>tpc2</i> deficient strain exhibits aberrant cell-type patterning and loss of distinct boundary between the prestalk/prespore regions.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusion</h3>\\n \\n <p>TPC2 is required for effective development and differentiation in <i>Dictyostelium</i> and supports autophagic cell death and cell-type patterning.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Significance</h3>\\n \\n <p>Decreased calcium due to deletion of <i>tpc2</i> inhibit autophagic flux.</p>\\n </section>\\n </div>\",\"PeriodicalId\":8859,\"journal\":{\"name\":\"Biology of the Cell\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2024-03-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biology of the Cell\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/boc.202300067\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biology of the Cell","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/boc.202300067","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Deletion of Dictyostelium tpc2 gene forms multi-tipped structures, regulates autophagy and cell-type patterning
Background Information
Two pore channels (TPCs) are voltage-gated ion channel superfamily members that release Ca2+ from acidic intracellular stores and are ubiquitously present in both animals and plants. Starvation initiates multicellular development in Dictyostelium discoideum. Increased intracellular calcium levels bias Dictyostelium cells towards the stalk pathway and thus we decided to analyze the role of TPC2 in development, differentiation, and autophagy.
Results
We showed TPC2 protein localizes in lysosome-like acidic vesicles and the in situ data showed stalk cell biasness. Deletion of tpc2 showed defective and delayed development with formation of multi-tipped structures attached to a common base, while tpc2OE cells showed faster development with numerous small-sized aggregates and wiry fruiting bodies. The tpc2OE cells showed higher intracellular cAMP levels as compared to the tpc2− cells while pinocytosis was found to be higher in the tpc2− cells. Also, TPC2 regulates cell-substrate adhesion and cellular morphology. Under nutrient starvation, deletion of tpc2 reduced autophagic flux as compared to Ax2. During chimera formation, tpc2− cells showed a bias towards the prestalk/stalk region while tpc2OE cells showed a bias towards the prespore/spore region. tpc2 deficient strain exhibits aberrant cell-type patterning and loss of distinct boundary between the prestalk/prespore regions.
Conclusion
TPC2 is required for effective development and differentiation in Dictyostelium and supports autophagic cell death and cell-type patterning.
Significance
Decreased calcium due to deletion of tpc2 inhibit autophagic flux.
期刊介绍：
The journal publishes original research articles and reviews on all aspects of cellular, molecular and structural biology, developmental biology, cell physiology and evolution. It will publish articles or reviews contributing to the understanding of the elementary biochemical and biophysical principles of live matter organization from the molecular, cellular and tissues scales and organisms.
This includes contributions directed towards understanding biochemical and biophysical mechanisms, structure-function relationships with respect to basic cell and tissue functions, development, development/evolution relationship, morphogenesis, stem cell biology, cell biology of disease, plant cell biology, as well as contributions directed toward understanding integrated processes at the organelles, cell and tissue levels. Contributions using approaches such as high resolution imaging, live imaging, quantitative cell biology and integrated biology; as well as those using innovative genetic and epigenetic technologies, ex-vivo tissue engineering, cellular, tissue and integrated functional analysis, and quantitative biology and modeling to demonstrate original biological principles are encouraged.
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