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In This Issue
Validating mouse model of Beckwith-Wiedemann syndrome
Disease Models & Mechanisms 2011 4: 709
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Mutations in the CDKN1C gene are associated with the childhood developmental disorder Beckwith-Wiedemann syndrome (BWS), whose main symptom is overgrowth of body and organ size. Cdkn1c-knockout mice do not show overgrowth at birth, casting doubt on the validity of mice as an appropriate BWS model. Now, Tunster et al. show that CDKN1C-deficient mouse foetuses do overgrow, but the effect is lost shortly before birth if the knockout foetuses are part of a large litter. This might have important implications for BWS underdiagnosis in non-singleton pregnancies in humans. Page 814

  • Written by editorial staff. © 2011. Published by The Company of Biologists Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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We are aware that the COVID-19 pandemic is having an unprecedented impact on researchers worldwide. The Editors of all The Company of Biologists’ journals have been considering ways in which we can alleviate concerns that members of our community may have around publishing activities during this time. Read about the actions we are taking at this time.

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Identification of MYOM2 as a candidate gene in hypertrophic cardiomyopathy and Tetralogy of Fallot, and its functional evaluation in the Drosophila heart

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C. elegans as a disease model

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Interview – Kim Landry-Truchon and Nicolas Houde

In an interview, first authors Kim Landry-Truchon and Nicolas Houde discuss their mouse model of the early stages of pleuropulmonary blastoma, reflecting on the implications of their work and the future of their field.

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