Coupling of growth rate and developmental tempo reduces body size heterogeneity in C. elegans.

Animals increase by orders of magnitude in volume during development. Therefore, small variations in growth rates among individuals could amplify to a large heterogeneity in size. By live imaging of C. elegans, we show that amplification of size heterogeneity is prevented by an inverse coupling of the volume growth rate to the duration of larval stages and does not involve strict size thresholds for larval moulting. We perturb this coupling by changing the developmental tempo through manipulation of a transcriptional oscillator that controls the duration of larval development. As predicted by a mathematical model, this perturbation alters the body volume. Model analysis shows that an inverse relation between the period length and the growth rate is an intrinsic property of genetic oscillators and can occur independently of additional complex regulation. This property of genetic oscillators suggests a parsimonious mechanism that counteracts the amplification of size differences among individuals during development

Forces directing germ-band extension in Drosophila embryos.

Body axis elongation by convergent extension is a conserved developmental process found in all metazoans. Drosophila embryonic germ-band extension is an important morphogenetic process during embryogenesis, by which the length of the germ-band is more than doubled along the anterior-posterior axis. This lengthening is achieved by typical convergent extension, i.e. narrowing the lateral epidermis along the dorsal-ventral axis and simultaneous extension along the anterior-posterior axis. Germ-band extension is largely driven by cell intercalation, whose directionality is determined by the planar polarity of the tissue and ultimately by the anterior-posterior patterning system. In addition, extrinsic tensile forces originating from the invaginating endoderm induce cell shape changes, which transiently contribute to germ-band extension. Here, we review recent progress in understanding of the role of mechanical forces in germ-band extension

The glucosyltransferase Xiantuan of the endoplasmic reticulum specifically affects E-Cadherin expression and is required for gastrulation movements in Drosophila

The majority of membrane and secreted proteins, including many developmentally important signalling proteins, receptors and adhesion molecules, are cotranslationally N-glycosylated in the endoplasmic reticulum. The structure of the N-glycan is invariant for all substrates and conserved in eukaryotes. Correspondingly, the enzymes are conserved, which successively assemble the glycan precursor from activated monosaccharides prior to transfer to nascent proteins. Despite the well-defined biochemistry, the physiological and developmental role of N-glycosylation and of the responsible enzymes has not been much investigated in metazoa. We identified a mutation in the Drosophila gene, xiantuan (xit, CG4542), which encodes one of the conserved enzymes involved in addition of the terminal glucose residues to the glycan precursor. xit is required for timely apical constriction of mesoderm precursor cells and ventral furrow formation in early embryogenesis. Furthermore, cell intercalation in the lateral epidermis during germband extension is impaired in xit mutants. xit affects glycosylation and intracellular distribution of E-Cadherin, albeit not the total amount of E-Cadherin protein. As depletion of E-Cadherin by RNAi induces a similar cell intercalation defect, E-Cadherin may be the major xit target that is functionally relevant for germband extension