Highlights in DD
Article first published online: 22 MAY 2008
Copyright © 2008 Wiley-Liss, Inc.
Volume 237, Issue 6, page fv, June 2008
How to Cite
Kiefer, J. (2008), Highlights in DD. Dev. Dyn., 237: fv. doi: 10.1002/dvdy.21532
- Issue published online: 22 MAY 2008
- Article first published online: 22 MAY 2008
“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 will spotlight 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.
Something to chew on (Dev Dyn237:1–17) A central tenet of developmental biology is that a tissue can influence the development of one adjacent. Think neural tube and somite, retina and lens. What is considered less often is that tissues that are functionally integrated, such as teeth and jaws, which together acquire and process food, must also coordinate their growth and development over time. In this review, Boughner and Hallgrimsson consider the processes that contribute to this aspect of development. Among their arguments is that the coordinated development of these two tissues is (1) the outcome of strong evolutionary selection, despite developing autonomous of one another and other surrounding tissues. (2) Because development of both of these tissues is tied to the timing of life “milestones,” such as weaning and sexual maturity, this suggests that their development is circadian in nature. (3) Development of the two tissues are not strictly in synch, suggesting that developmental timing for each tissue is under the control of independent clocks peripheral to the master circadian clock. The authors' detailed presentation of supporting evidence makes their model easy to swallow.
Totally (micro)tubular (Dev Dyn237:91–96) The right experimental approach can snap into focus something that had been unclear. The primitive streak is dynamic: cells along the streak ingress inward, a process that organizes the three germ layers. Less obvious is how dynamics differ along the primitive streak. By adapting a fixation procedure designed to preserve microtubules for use on whole chick embryos, the authors find that the organization of the microtubule cytoskeleton differs in cells along the length of the primitive streak. Microtubule arrays in cells at the anterior tip are disorganized, while those in the middle region of the streak are polarized toward the direction of migration. Strikingly, cells with polarized microtubule arrays assemble into groups of six or more, forming eye-catching “rosettes”. Three-dimensional reconstruction reveals that cell tips, rich in actin, at the rosette center protrude toward the hypoblast. The findings suggest that primitive streak cells rearrange their microtubule cytoskeleton in response to undefined extracellular cues. Furthermore, the higher order cell shape changes may facilitate ingression of groups of cells. As they say, a picture is worth a thousand words.
Interneuron adolescence (Dev Dyn237:393–402) Like adolescence and bad acne, cell cycle exit and cell differentiation are tightly coupled, yet separable, events. In uncovering a role for Prox1, the vertebrate ortholog of Drosophila prospero, Misra et al. show that the gene links these two cellular events. This is supported primarily by three lines of evidence. First, it is transiently expressed in interneuron progenitors after mitotic exit and before differentiation. Second, forced expression of the gene triggers cell cycle exit and expression of the pan-neuronal marker β-tubulin. Third, misexpression of the neurogenic genes Ngn2 or Mash1 triggers Prox1 expression, and blocking Prox1 by RNAi during those experiments inhibits neurogenesis. Both findings suggest Prox1 is a requisite component downstream of Ngn2 or Mash1. Of interest, its interneuron-specific expression seems to be contrary to the motorneuron fate. Prox1 is repressed by Olig2, a gene that promotes motorneuron fate, and is up-regulated in mice deficient in Olig2. Taken together these data are evidence that Prox1 pushes a cell into interneuron adolescence: the cell has begun to acquire its own identity, but needs further instruction before it can achieve independence.