Here are the highlights from the current issue of Development:
ECM: bridging the gap between germ layers
The extracellular matrix (ECM) plays crucial roles during morphogenesis but how it is assembled and patterned in vivo is poorly understood. Here, Yuki Sato, Rusty Lansford and colleagues investigate this by examining the distribution of the ECM component fibronectin (FN) in quail embryos (p. 281). They reveal that FN fibrils form pillars that span the gap between somites and the endoderm. The tissue-specific depletion of FN reveals that both the somites and endoderm provide FN that contributes to these pillars. The authors also observe filopodia-like structures that extend from the basal surface of somatic epithelial cells and are oriented along FN pillars. The formation of these filopodia influences the formation of FN pillars, while the polymerisation of FN is shown to modulate both pillar formation and filopodial elongation. Importantly, both structures are required for proper somite morphogenesis. Finally, the researchers report that blood flow in the nascent dorsal aorta (DA), which is located between the somites and endoderm, controls FN pillar distribution; disruption of DA formation, or occlusion of the DA, leads to a scattered distribution of FN pillars. Together, these findings suggest that pulsations from the DA help establish FN pillars that bridge the somite-endoderm gap and potentially aid communication between these tissues.
Brainy roles for cilia and mTORC1
During vertebrate brain development, neurons and glia arise from a population of self-renewing radial glial cells (RGCs) that contact the cerebral ventricles and bear a primary cilium. Primary cilia are known to play crucial roles in signalling but it is not clear if they are required for morphogenesis. Now, on p. 201, Nathalie Spassky and co-workers show that primary cilia on RGCs are essential for proper ventricular morphogenesis in mice. They first report that ciliary mutant mice exhibit enlarged lateral ventricles (ventriculomegaly) and reduced cortical thickness. The absence of primary cilia also leads to an increase in the size of RGC apical domains. This apical endfoot enlargement, the authors report, is associated with spindle orientation defects and is caused by upregulation of the mTORC1 pathway. Accordingly, treatment with rapamycin – an mTORC1 inhibitor – prevents apical domain enlargement in ciliary mutants and rescues their ventriculomegaly phenotype. Overall, this study reveals a new role for the mTORC1 pathway in regulating ventricle morphogenesis and corticogenesis, suggesting that it constitutes a new potential therapeutic target for the treatment of ventriculomegaly.
Getting to the root of brassinosteroid function
The plant hormone brassinosteroid (BR), which signals through its receptors BR INSENSITIVE 1 (BRI1), BRI1-LIKE 1 (BRL1) and BRL3, is known to regulate hypocotyl elongation but how it functions in the root is less clear. In this issue, Christian Hardtke and colleagues assess the role of BR during cell differentiation in the Arabidopsis root (p. 272). They first show that bri1 brl1 brl3 triple mutants display protophloem differentiation defects. These defects cannot be rescued by activating BR signalling in adjacent cell files, suggesting that BR acts in a cell-autonomous manner to control protophloem differentiation. Triple mutants also exhibit a small meristem, and the authors show that this can be explained by reduced cell elongation that, together with increased formative divisions in the radial dimension, contributes to the overall reduction in root growth observed in these mutants. Finally, the researchers demonstrate that the protophloem-specific activation of BR signalling can rescue all major aspects of the triple mutant phenotype, thus uncovering a new facet of the non-cell-autonomous effects of BR signalling. Based on these and other findings, the authors propose that BR perception in the protophloem is sufficient to systemically convey BR action within the root meristem.
Primate embryogenesis predicts the hallmarks of human naïve pluripotency
Planar cell polarity in moving cells: think globally, act locally