{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T19:25:44Z","timestamp":1761765944919,"version":"3.41.2"},"reference-count":87,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2016,4,1]],"date-time":"2016-04-01T00:00:00Z","timestamp":1459468800000},"content-version":"vor","delay-in-days":456,"URL":"http:\/\/www.biologists.com\/user-licence-1-1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,1,1]]},"abstract":"<jats:p>A leading cause of human birth defects is the incomplete fusion of tissues, often manifested in the palate, heart, or neural tube. To investigate the molecular control of tissue fusion, embryonic dorsal closure and pupal thorax closure in Drosophila are useful experimental models. We find that Pvr mutants have defects in dorsal midline closure with incomplete amnioserosa internalization and epidermal zippering, as well as cardia bifida. These defects are relatively mild in comparison to those seen with other signaling mutants such as the JNK pathway, and we demonstrate that JNK signaling is not perturbed by altering Pvr receptor tyrosine kinase activity. Rather, modulation of Pvr levels in the ectoderm has an impact on PIP3 membrane accumulation consistent with a link to PI3K signal transduction. Polarized PI3K activity influences protrusive activity from the epidermal leading edge and protrusion area changes in accord with Pvr signaling intensity, providing a possible mechanism to explain Pvr mutant phenotypes. Tissue specific rescue experiments indicate a partial requirement in epithelial tissue, but confirm the essential role of Pvr in the hemocytes for embryonic survival. Taken together, we argue that inefficient removal of the internalizing amnioserosa tissue by mutant hemocytes coupled with impaired midline zippering of mutant epithelium creates a situation in some embryos where dorsal midline closure is incomplete. Based on these observations, we suggest that efferocytosis (corpse clearance) could contribute to proper tissue closure and thus may underlie some congenital birth defects.<\/jats:p>","DOI":"10.1242\/dev.122226","type":"journal-article","created":{"date-parts":[[2015,8,21]],"date-time":"2015-08-21T01:39:13Z","timestamp":1440121153000},"source":"Crossref","is-referenced-by-count":12,"title":["Pvr receptor tyrosine kinase promotes tissue closure by coordinating corpse removal and epidermal zippering"],"prefix":"10.1242","author":[{"given":"Rebecca A.","family":"Garlena","sequence":"first","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ashley L.","family":"Lennox","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA"},{"name":"Present address: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lewis R.","family":"Baker","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Trish E.","family":"Parsons","sequence":"additional","affiliation":[{"name":"Center for Craniofacial and Dental Genetics, Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seth M.","family":"Weinberg","sequence":"additional","affiliation":[{"name":"Center for Craniofacial and Dental Genetics, Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Beth E.","family":"Stronach","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"237","reference":[{"key":"2021042608070609900_DEV122226C1","doi-asserted-by":"publisher","first-page":"2023","DOI":"10.1242\/dev.045088","article-title":"The leading edge during dorsal closure as a model for epithelial plasticity: Pak is required for recruitment of the Scribble complex and septate junction formation","volume":"137","author":"Bahri","year":"2010","journal-title":"Development"},{"key":"2021042608070609900_DEV122226C2","doi-asserted-by":"publisher","first-page":"567","DOI":"10.1534\/genetics.108.096461","article-title":"The PP2C Alphabet is a negative regulator of stress-activated protein kinase signaling in Drosophila","volume":"181","author":"Baril","year":"2009","journal-title":"Genetics"},{"key":"2021042608070609900_DEV122226C3","doi-asserted-by":"publisher","first-page":"2743","DOI":"10.1242\/dev.045872","article-title":"Cytoskeletal dynamics and supracellular organisation of cell shape fluctuations during dorsal closure","volume":"137","author":"Blanchard","year":"2010","journal-title":"Development"},{"key":"2021042608070609900_DEV122226C4","doi-asserted-by":"crossref","first-page":"401","DOI":"10.1242\/dev.118.2.401","article-title":"Targeted gene expression as a means of altering cell fates and generating dominant phenotypes","volume":"118","author":"Brand","year":"1993","journal-title":"Development"},{"key":"2021042608070609900_DEV122226C5","doi-asserted-by":"publisher","first-page":"1307","DOI":"10.1002\/bies.20137","article-title":"Finally, a sense of closure? 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