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Subject collection: Developmental Disorders

  • RESEARCH ARTICLE
    Six1 proteins with human branchio-oto-renal mutations differentially affect cranial gene expression and otic development
    Ankita M. Shah, Patrick Krohn, Aparna B. Baxi, Andre L. P. Tavares, Charles H. Sullivan, Yeshwant R. Chillakuru, Himani D. Majumdar, Karen M. Neilson, Sally A. Moody
    Disease Models & Mechanisms 2020 13: dmm043489 doi: 10.1242/dmm.043489 Published 3 March 2020

    Summary: Branchio-otic/branchio-oto-renal syndromes result in craniofacial defects including deafness. Four of the known human SIX1 mutations cause differential changes in craniofacial gene expression and otic morphology when expressed in Xenopus embryos.

  • RESOURCE ARTICLE
    Establishment and validation of an endoplasmic reticulum stress reporter to monitor zebrafish ATF6 activity in development and disease
    Eric M. Clark, Hannah J. T. Nonarath, Jonathan R. Bostrom, Brian A. Link
    Disease Models & Mechanisms 2020 13: dmm041426 doi: 10.1242/dmm.041426 Published 28 January 2020

    Summary: In this study, we validate transgenic zebrafish generated to specifically report the activity of ATF6, representing a major branch of the endoplasmic reticulum stress pathway with functions in development and disease.

  • RESEARCH ARTICLE
    Oral administration of a synthetic vinyl-ether plasmalogen normalizes open field activity in a mouse model of rhizomelic chondrodysplasia punctata
    Wedad Fallatah, Tara Smith, Wei Cui, Dushmanthi Jayasinghe, Erminia Di Pietro, Shawn A. Ritchie, Nancy Braverman
    Disease Models & Mechanisms 2020 13: dmm042499 doi: 10.1242/dmm.042499 Published 24 January 2020

    Summary: This article shows, for the first time, that a synthetic vinyl-ether plasmalogen is orally bioavailable and bioactive in vivo following administration in animals.

  • RESEARCH ARTICLE
    A model for reticular dysgenesis shows impaired sensory organ development and hair cell regeneration linked to cellular stress
    Alberto Rissone, Erin Jimenez, Kevin Bishop, Blake Carrington, Claire Slevin, Stephen M. Wincovitch, Raman Sood, Fabio Candotti, Shawn M. Burgess
    Disease Models & Mechanisms 2019 12: dmm040170 doi: 10.1242/dmm.040170 Published 20 December 2019

    Summary: A zebrafish model of reticular dysgenesis reveals hair cell developmental deficits that can be partially rescued by antioxidants, pointing to their potential use as a therapeutic treatment for reticular dysgenesis patients.

  • RESEARCH ARTICLE
    Regulation of terminal hypertrophic chondrocyte differentiation in Prmt5 mutant mice modeling infantile idiopathic scoliosis
    Zhaoyang Liu, Janani Ramachandran, Steven A. Vokes, Ryan S. Gray
    Disease Models & Mechanisms 2019 12: dmm041251 doi: 10.1242/dmm.041251 Published 17 December 2019

    Summary: Loss of Prmt5 in osteochondral progenitors impairs terminal hypertrophic chondrocyte differentiation, leading to defects in endochondral bone formation and models infantile idiopathic scoliosis in mouse.

  • RESEARCH ARTICLE
    Cellular mechanisms underlying Pax3-related neural tube defects and their prevention by folic acid
    Sonia Sudiwala, Alexandra Palmer, Valentina Massa, Alan J. Burns, Louisa P. E. Dunlevy, Sandra C. P. de Castro, Dawn Savery, Kit-Yi Leung, Andrew J. Copp, Nicholas D. E. Greene
    Disease Models & Mechanisms 2019 12: dmm042234 doi: 10.1242/dmm.042234 Published 22 November 2019

    Summary: Neural tube defects in a folic-acid-responsive, folate-sensitive mouse model are associated with a localised proliferation defect in the neuroepithelium. Supplemental folic acid stimulates progression through S phase to correct this abnormality.

  • RESEARCH ARTICLE
    Impaired neural differentiation and glymphatic CSF flow in the Ccdc39 rat model of neonatal hydrocephalus: genetic interaction with L1cam
    A. Scott Emmert, Eri Iwasawa, Crystal Shula, Preston Schultz, Diana Lindquist, R. Scott Dunn, Elizabeth M. Fugate, Yueh-Chiang Hu, Francesco T. Mangano, June Goto
    Disease Models & Mechanisms 2019 12: dmm040972 doi: 10.1242/dmm.040972 Published 21 November 2019

    Summary: Glymphatic CSF circulation and development of the cerebral cortex are impaired in our new genetic rat model of neonatal hydrocephalus with the onset of parenchymal inflammation and hemorrhage.

  • RESEARCH ARTICLE
    Perturbation of the titin/MURF1 signaling complex is associated with hypertrophic cardiomyopathy in a fish model and in human patients
    Yuta Higashikuse, Nishant Mittal, Takuro Arimura, Sung Han Yoon, Mayumi Oda, Hirokazu Enomoto, Ruri Kaneda, Fumiyuki Hattori, Takeshi Suzuki, Atsushi Kawakami, Alexander Gasch, Tetsushi Furukawa, Siegfried Labeit, Keiichi Fukuda, Akinori Kimura, Shinji Makino
    Disease Models & Mechanisms 2019 12: dmm041103 doi: 10.1242/dmm.041103 Published 15 November 2019

    Summary: The authors identified and characterized a medaka mutation in titin that leads to a phenotype similar to hypertrophic cardiomyopathy. Similar mutations were also observed in human patients.

  • RESEARCH ARTICLE
    Novel mouse model of encephalocele: post-neurulation origin and relationship to open neural tube defects
    Ana Rolo, Gabriel L. Galea, Dawn Savery, Nicholas D. E. Greene, Andrew J. Copp
    Disease Models & Mechanisms 2019 12: dmm040683 doi: 10.1242/dmm.040683 Published 14 November 2019

    Summary: Encephalocele is a severe congenital brain defect that arises after neural tube closure, but can share a common genetic cause with defects of cranial and spinal neural tube closure.

  • RESEARCH ARTICLE
    Lack of whey acidic protein (WAP) four-disulfide core domain protease inhibitor 2 (WFDC2) causes neonatal death from respiratory failure in mice
    Kuniko Nakajima, Michio Ono, Uroš Radović, Selma Dizdarević, Shin-ichi Tomizawa, Kazushige Kuroha, Go Nagamatsu, Ikue Hoshi, Risa Matsunaga, Takayuki Shirakawa, Takeyuki Kurosawa, Yasunari Miyazaki, Masahide Seki, Yutaka Suzuki, Haruhiko Koseki, Masataka Nakamura, Toshio Suda, Kazuyuki Ohbo
    Disease Models & Mechanisms 2019 12: dmm040139 doi: 10.1242/dmm.040139 Published 12 November 2019

    Summary: Wfdc2 is vitally important in preventing atelectasis and dysfunction of barrier mechanisms such as mucociliary clearance, intercellular junction formation and anti-inflammatory activity.

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