Next Article in Journal / Special Issue
Dissecting the Role of the Extracellular Matrix in Heart Disease: Lessons from the Drosophila Genetic Model
Previous Article in Journal
Minimising Stress for Patients in the Veterinary Hospital: Why It Is Important and What Can Be Done about It
Previous Article in Special Issue
Coronary Artery Anomalies in Animals
Article Menu
Issue 2 (June) cover image

Export Article

Open AccessArticle
Vet. Sci. 2017, 4(2), 23; doi:10.3390/vetsci4020023

Mapping Heart Development in Flies: Src42A Acts Non-Autonomously to Promote Heart Tube Formation in Drosophila

1
Department of Biology, Taylor University, 236 West Reade Ave., Upland, IN 46989, USA
2
Department of Biology, McMaster University, 1280 Main St. W., Hamilton, ON L8S 4K1, Canada
*
Author to whom correspondence should be addressed.
Academic Editors: Sonja Fonfara and Lynne O’Sullivan
Received: 25 October 2016 / Revised: 27 November 2016 / Accepted: 7 December 2016 / Published: 24 April 2017
(This article belongs to the Special Issue Comparison of Cardiovascular Systems and Diseases Across Species)
View Full-Text   |   Download PDF [20997 KB, uploaded 24 April 2017]   |  

Abstract

Congenital heart defects, clinically identified in both small and large animals, are multifactorial and complex. Although heritable factors are known to have a role in cardiovascular disease, the full genetic aetiology remains unclear. Model organism research has proven valuable in providing a deeper understanding of the essential factors in heart development. For example, mouse knock-out studies reveal a role for the Integrin adhesion receptor in cardiac tissue. Recent research in Drosophila melanogaster (the fruit fly), a powerful experimental model, has demonstrated that the link between the extracellular matrix and the cell, mediated by Integrins, is required for multiple aspects of cardiogenesis. Here we test the hypothesis that Integrins signal to the heart cells through Src42A kinase. Using the powerful genetics and cell biology analysis possible in Drosophila, we demonstrate that Src42A acts in early events of heart tube development. Careful examination of mutant heart tissue and genetic interaction data suggests that Src42A’s role is independent of Integrin and the Integrin-related Focal Adhesion Kinase. Rather, Src42A acts non-autonomously by promoting programmed cell death of the amnioserosa, a transient tissue that neighbors the developing heart. View Full-Text
Keywords: heart; Drosophila; model organism; Integrin; Src42A; FAK; genetics; amnioserosa heart; Drosophila; model organism; Integrin; Src42A; FAK; genetics; amnioserosa
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Vanderploeg, J.; Jacobs, J.R. Mapping Heart Development in Flies: Src42A Acts Non-Autonomously to Promote Heart Tube Formation in Drosophila. Vet. Sci. 2017, 4, 23.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Vet. Sci. EISSN 2306-7381 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top