{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T02:29:13Z","timestamp":1775096953995,"version":"3.50.1"},"reference-count":43,"publisher":"The Company of Biologists","issue":"12","license":[{"start":{"date-parts":[[2022,12,6]],"date-time":"2022-12-06T00:00:00Z","timestamp":1670284800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"name":"National Cancer Institute","award":["F30CA257383"],"award-info":[{"award-number":["F30CA257383"]}]},{"name":"Human Frontiers Science Program","award":["LT000127\/2016-L"],"award-info":[{"award-number":["LT000127\/2016-L"]}]},{"DOI":"10.13039\/100000011","name":"Howard Hughes Medical Institute","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100000011","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"crossref","award":["R01GM121597"],"award-info":[{"award-number":["R01GM121597"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100007259","name":"Stony Brook University","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007259","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,12,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:p>Development of the Caenorhabditis elegans reproductive tract is orchestrated by the anchor cell (AC). This occurs in part through a cell invasion event that connects the uterine and vulval tissues. Several key transcription factors regulate AC invasion, such as EGL-43, HLH-2, and NHR-67. Specifically, these transcription factors function together to maintain the post-mitotic state of the AC, a requirement for AC invasion. Recently, a mechanistic connection has been made between loss of EGL-43 and AC cell-cycle entry. The current model states that EGL-43 represses LIN-12 (Notch) expression to prevent AC proliferation, suggesting that Notch signaling has mitogenic effects in the invasive AC. To reexamine the relationship between EGL-43 and LIN-12, we first designed and implemented a heterologous co-expression system called AIDHB that combines the auxin-inducible degron (AID) system of plants with a live cell-cycle sensor based on human DNA helicase B (DHB). After validating AIDHB using AID-tagged GFP, we sought to test it by using AID-tagged alleles of egl-43 and lin-12. Auxin-induced degradation of either EGL-43 or LIN-12 resulted in the expected AC phenotypes. Lastly, we seized the opportunity to pair AIDHB with RNAi to co-deplete LIN-12 and EGL-43, respectively, which revealed that LIN-12 is not required for AC proliferation following loss of EGL-43.<\/jats:p>","DOI":"10.1242\/bio.059668","type":"journal-article","created":{"date-parts":[[2022,11,29]],"date-time":"2022-11-29T13:21:08Z","timestamp":1669728068000},"source":"Crossref","is-referenced-by-count":4,"title":["Reevaluating the relationship between EGL-43 (EVI1) and LIN-12 (Notch) during <i>C. elegans<\/i> anchor cell invasion"],"prefix":"10.1242","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1178-7139","authenticated-orcid":false,"given":"Michael A. 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