Highlights in DD
Article first published online: 11 FEB 2010
Copyright © 2010 Wiley-Liss, Inc.
Volume 239, Issue 3, page fvi, March 2010
How to Cite
Kiefer, J. C. (2010), Highlights in DD. Dev. Dyn., 239: fvi. doi: 10.1002/dvdy.22214
- Issue published online: 11 FEB 2010
- Article first published online: 11 FEB 2010
“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.
Green inspiration (Primer and Interviews: Gene Regulation in Arabidopsis thaliana by Julie C. Kiefer, Dev Dyn238:2449–2458). The differences between plants and animals are obvious, but are you familiar with their similarities? This primer on Arabidopsis thaliana traces the reasons behind this weed's rapid rise to super-stardom as a model system, and compares and contrasts gene regulation (including transcription factors, signal transduction, chromatin regulators, and small RNAs) in Arabidopsis and animals. Brief descriptions of other established and up and coming developmental plant models are also included. Interviews with Arabidopsis systems biologist Philip Benfey, PhD, and regeneration biologist Kenneth Birnbaum, PhD, reveal methods and ideas that may stir the animal biologist's imagination. A walk among garden plants can be inspiring, and so too can a read through the plant literature.
Partners in crime (Selective Interaction Between Trf3 and Taf3 Required for Early Development and Hematopoiesis by Daniel O. Hart, Manas K. Santra, Tamal Raha, and Michael R. Green, Dev Dyn238:2540–2549). Sometimes you need just the right tool to do the job. TATA-box binding protein (TBP) related factor 3 (TRF3) regulates transcription of mespa, a gene required for normal embryonic development and commitment of mesoderm to the hematopoietic lineage. Puzzlingly, previous work shows that TRF3 does not work through the general transcription factor TFIID, as other TRFs do. Has TRF3 found another partner to accomplish these tasks? Here, the authors test the hypothesis that, as has been shown in differentiated muscle, TRF3 cooperates with TBP associated factor 3 (TAF3). Supporting this idea, chromatin immunoprecipitation (ChIP) experiments demonstrate that Taf3 and Trf3, but not Tbp, bind to the mespa promoter. Furthermore, taf3 MO-treated embryos phenocopy trf3 MO-treated embryos, and are rescued by injection of mespa mRNA. Importantly, tagged Trf3 co-immunoprecipitates with tagged Taf3, as would be expected if the two proteins form a complex. The physical interaction is disrupted when two residues in a conserved region of the Trf3 C-terminus are mutated (Trf3[SDM1]). The residues are also functionally important because Trf3(SDM1) fails to rescue trf3 MO-treated embryos. Vertebrates apparently know a good thing when they see it—initial in vitro experiments demonstrate that the Taf3/Trf3 functional interaction is also conserved in mouse hematopoiesis.
About face (Craniofacial Skeletal Defects of Adult Zebrafish glypican 4 [knypek] Mutants by Elizabeth E. LeClair, Stephanie R. Mui, Angela Huang, Jolanta M. Topczewska, and Jacek Topczewski, Dev Dyn238:2550–2563). Zebrafish glypican 4 (gpc4)—an extracellular proteoglycan that modulates Wnt/PCP signaling—is perhaps best known as a regulator of convergence and extension movements in the gastrulating embryo. Injection of gpc4 mRNA into gpc4−/− (knypek) mutants rescues convergence and extension, but the larvae develop with skull and jaw defects, suggesting a role for the gene in craniofacial development. To characterize these larval morphological defects and follow them throughout ontogeny, LeClair et al. rescued gpc4−/− larvae and then grew them for up to 1 year. In larvae, rod-shaped pharyngeal cartilage elements, including the symplectic, appear shortened and thickened. Affected symplectic chondrocytes fail to ossify in juveniles, resulting in a loss of the corresponding bones in the adult. In some animals, morphological rearrangement of the bones and cartilages surrounding the symplectic compensate for this loss, allowing for a functional jaw. At the cellular level, chondrocytes in affected elements are rounded and disorganized. These observations lead to the hypothesis that Gpc4 operates similarly in cartilage assembly as in convergence and extension, by regulating the cell elongation and/or cell–cell intercalation behaviors necessary to generate a columnar orientation of chondrocytes in craniofacial elements and the cartilage growth plate.