Highlights in DD
Version of Record online: 19 MAR 2009
Copyright © 2009 Wiley-Liss, Inc.
Volume 238, Issue 4, page fv, April 2009
How to Cite
Kiefer, J. (2009), Highlights in DD. Dev. Dyn., 238: fv. doi: 10.1002/dvdy.21897
- Issue online: 19 MAR 2009
- Version of Record online: 19 MAR 2009
‘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.
Calculating what's left (Fluid dynamics of nodal flow and left-right patterning in development by Julyan H.E. Cartwright, Nicolas Piro, Oreste Piro, Idan Tuval, Dev Dyn237:3477–3490) Like it or not, most biological phenomena cannot be adequately explained without the help of physics. Luckily for the physics-phobe, there are gifted teachers such as Cartwright and colleagues who are exceptionally skilled at explaining biology's numerical roots. This review covers their and others' work modeling the fluid dynamics behind nodal flow–fluid flow induced by monocilia within the node, one of the earliest steps in establishing vertebrate left–right asymmetry. In the interest of examining models with predictive power, they discuss what happens when as of yet experimentally untested variables are included in fluid dynamical models. Biological concepts are nimbly intertwined with the derivation of models that can be used to understand them, giving even the most mathematically challenged something onto which they can grasp.
Change of heart (Cellular nonmuscle myosins NMHC-IIA and NMHC-IIB and vertebrate heart looping by Wenge Lu, Steven H. Seeholzer, Mingda Han, Anne-Sophie Arnold, Maria Serrano, Barbara Garita, Nancy J. Philp, Cassandra Farthing, Peter Steele, Jizhen Chen, Kersti K. Linask, Dev Dyn237:3557–3564) Galanin is a neuropeptide, well known for regulating various nervous system functions, such as metabolism and regulation of food intake. Therefore, it is surprising that Schweickert and colleagues found that Gal, the gene that encodes Galanin, is asymmetrically expressed in the linear heart tube, and is later localized to the second pacemaker, the atrioventricular node and ring. Furthermore, like asymmetric expression of left–right (LR) patterning gene Nodal, and downstream genes Lefty2 and Pitx2c in the lateral plate mesoderm (LPM) in the early embryo, left-sided heart Gal expression at later stages is dependent on leftward flow of cilia in the posterior notochord (commonly termed as node). This finding demonstrates that Gal is regulated by the LR pathway. Therefore, it is surprising that Gal heart expression remains unchanged in mutants for the Nodal co-receptor cryptic, even though expression of Nodal cascade genes disappears in the LPM. Also surprising is that asymmetric heart expression of Pitx2c also remains unchanged in half of cryptic homozygotes. This discovery led the authors to hypothesize that asymmetric gene expression in the heart is cryptic independent. Neither Galanin nor cryptic are behaving as expected—perhaps they had a change of heart.
MANning the barrier (Man1, an inner nuclear membrane protein, regulates left-right axis formation by controlling nodal signaling in a node-independent manner by Akihiko Ishimura, Shinsuke Chida, Shin-lchi Osada, Dev Dyn237:3565–3576) During specification of the left–right axis, the midline acts as a barrier that keeps asymmetrically expressed signals from becoming bilateral. Here, Ishimura et al., provide evidence for the first time that Man1, an inner nuclear membrane protein, regulates activity of a midline barrier. Transgenic mice bearing truncated MAN1 that lacks an R-SMAD interacting domain (R-SMADs are downstream effectors of TGFβ family signaling), show bilateral expression of the left–right determination gene Nodal, and downstream genes Lefty2 and Pitx2. Of interest, ectopic expression of the three genes occurs despite that Lefty1, a marker for the midline barrier, is still present. How could this be? One possible answer lies in the discovery that expression of coreceptors for Nodal, Cryptic and Cripto, are up-regulated. The event may enhance competence for Nodal signaling. Another possibility stems from their finding that bilateral Nodal expression is maintained in Man1 mutants crossed with Nodal hypomorphs, despite that these double mutants lack a node, and thus early node-derived Nodal. This means that, instead of under the control of node-derived Nodal, ectopic Nodal may be controlled by an unknown molecule that is derepressed in a Man1 mutant background. One candidate is Bmp2, whose expression is also augmented in Man1 mutants. The observation that Man1 is transiently expressed in the posterior midline bolsters the idea that the gene also directly or indirectly regulates activity of a midline barrier.