Highlights in DD
Article first published online: 25 SEP 2012
Copyright © 2012 Wiley Periodicals, Inc.
Volume 241, Issue 10, October 2012
How to Cite
Kiefer, J. C. (2012), Highlights in DD. Dev. Dyn., 241: n/a. doi: 10.1002/dvdy.23848
- Issue published online: 25 SEP 2012
- Article first published online: 25 SEP 2012
“Highlights” calls attention to exciting advances in developmental biology that have recently been reported in Developmental Dynamics. Development is a broad field encompassing many important areas. To reflect this fact, the section spotlights significant discoveries that occur across the entire spectrum of developmental events and problems: from new experimental approaches, to novel interpretations of results, to noteworthy findings utilizing different developmental organisms.
Unraveling the truth (The ENU-induced cetus Mutation Reveals an Essential Role of the DNA Helicase DDX11 for Mesoderm Development During Early Mouse Embryogenesis by Christina D. Cota and Maréa J. García-García, Dev Dyn 241:1249–1259) The ENU-induced recessive cetus mutation initially caught the interest of Cota and Garcé a-Garcé a because homozygous mutants arrest before E8.5 with severe developmental defects. Here, the authors find that the mutation lies within the well-conserved motif V of the DNA helicase DDX11, creating a null allele. Embryonic characterization shows, among other defects, the unusual phenotype of an absence of somitic tissue while other mesodermal derivatives are normally specified to their respective fates. TUNEL staining demonstrates widespread apoptosis throughout the embryo, but somitic mesodermal cells completely die off before or just after specification to the somitic fate. DDX11 is expressed ubiquitously throughout the embryo and is required for sister chromatid cohesion during S-phase, and participates in DNA repair, suggesting that the embryonic phenotypes originate from genomic instability. The authors speculate that enhanced sensitivity of somites toward genomic instability may be due to their high proliferative index, which has been proposed to hamper DNA damage repair. This realization could provide insights into the etiology of human diseases, including xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy, that stem from mutations in the highly conserved motif V region in other DNA helicases.
Measuring inequality (A Universal Analysis Tool for the Detection of Asymmetric Signal Distribution in Microscopic Images by Maja Matis, Jeffrey D. Axelrod, and Milos Galic, Dev Dyn 241:1301–1309) Sometimes inequality isn't such a bad thing. Subcellular distributions of planar cell polarity (PCP) proteins are one-sided for a reason—their asymmetric localization drive diverse cellular processes including directed cell movements during convergent extension, and proper positioning of sensory cells and cilia. Commonly used methods for quantifying asymmetric distribution include measuring the distance or angle between the structure of interest and the center of a cell-internal reference point. However, resulting measurements are at times inaccurate due to variability in reference point localization within individual cells, or irregularity in the shape of the investigated structures that make it difficult. Overcoming these limitations, Matis and colleagues show that spatial cross-correlation of the fluorescent intensities of the structure of interest and cellular reference can be used to reliably measure asymmetric distribution of PCP proteins in abdominal epithelia in live Drosophila. Furthermore, the method can also be adapted to measure cells as they contort their shape and and/or size during developmental processes. These findings combined with the fact that the assay is freely accessible as a plugin for ImageJ (JACoP—Just Another Colocalization Plugin) and as a function in Matlab (http://www.stanford.edu/group/axelrodlab/code) makes it worth a look–but that's just my bias.