Monica M Macharios, Yasmine D Hernandez, Peter C Breen, Robert H Dowen
{"title":"在秀丽隐杆线虫中,卵黄原蛋白的丧失会造成适合度的劣势,但不会影响后代的大小。","authors":"Monica M Macharios, Yasmine D Hernandez, Peter C Breen, Robert H Dowen","doi":"10.17912/micropub.biology.001789","DOIUrl":null,"url":null,"abstract":"<p><p>Organismal homeostasis relies on balancing cellular metabolic decisions with environmental conditions, especially during reproduction. Using <i>Caenorhabditis elegans</i> , we tested whether vitellogenesis, or the deposition of lipid-rich yolk into oocytes, is required for reproductive output and metabolic balance by creating a strain lacking all six vitellogenin genes ( <i>vit-1-6</i> ). This mutant produced embryos with reduced lipid content compared to wild-type, but the total brood size remained unaffected, unlike the <i>rme-2</i> mutant, which lacks the yolk receptor. However, progeny survival during L1 starvation was impaired in <i>vit-1-6</i> animals. This strain offers a new model for studying how vitellogenesis impacts reproductive and organismal fitness.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461288/pdf/","citationCount":"0","resultStr":"{\"title\":\"Loss of the vitellogenins confers a fitness disadvantage but does not impact brood size in <i>C. elegans</i>.\",\"authors\":\"Monica M Macharios, Yasmine D Hernandez, Peter C Breen, Robert H Dowen\",\"doi\":\"10.17912/micropub.biology.001789\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Organismal homeostasis relies on balancing cellular metabolic decisions with environmental conditions, especially during reproduction. Using <i>Caenorhabditis elegans</i> , we tested whether vitellogenesis, or the deposition of lipid-rich yolk into oocytes, is required for reproductive output and metabolic balance by creating a strain lacking all six vitellogenin genes ( <i>vit-1-6</i> ). This mutant produced embryos with reduced lipid content compared to wild-type, but the total brood size remained unaffected, unlike the <i>rme-2</i> mutant, which lacks the yolk receptor. However, progeny survival during L1 starvation was impaired in <i>vit-1-6</i> animals. This strain offers a new model for studying how vitellogenesis impacts reproductive and organismal fitness.</p>\",\"PeriodicalId\":74192,\"journal\":{\"name\":\"microPublication biology\",\"volume\":\"2025 \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-09-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461288/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"microPublication biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.17912/micropub.biology.001789\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"microPublication biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17912/micropub.biology.001789","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
Loss of the vitellogenins confers a fitness disadvantage but does not impact brood size in C. elegans.
Organismal homeostasis relies on balancing cellular metabolic decisions with environmental conditions, especially during reproduction. Using Caenorhabditis elegans , we tested whether vitellogenesis, or the deposition of lipid-rich yolk into oocytes, is required for reproductive output and metabolic balance by creating a strain lacking all six vitellogenin genes ( vit-1-6 ). This mutant produced embryos with reduced lipid content compared to wild-type, but the total brood size remained unaffected, unlike the rme-2 mutant, which lacks the yolk receptor. However, progeny survival during L1 starvation was impaired in vit-1-6 animals. This strain offers a new model for studying how vitellogenesis impacts reproductive and organismal fitness.