Neuronal calmodulin levels are controlled by CAMTA transcription factors.

The ubiquitous Ca sensor calmodulin (CaM) binds and regulates many proteins, including ion channels, CaM kinases, and calcineurin, according to Ca-CaM levels. What regulates neuronal CaM levels, is, however, unclear. CaM-binding transcription activators (CAMTAs) are ancient proteins expressed broadly in nervous systems and whose loss confers pleiotropic behavioral defects in flies, mice, and humans.

Novel cytokinetic ring components drive negative feedback in cortical contractility.

Actomyosin cortical contractility drives many cell shape changes including cytokinetic furrowing. While positive regulation of contractility is well characterized, counterbalancing negative regulation and mechanical brakes are less well understood. The small GTPase RhoA is a central regulator, activating cortical actomyosin contractility during cytokinesis and other events.

The plakin domain of VAB-10/plectin acts as a hub in a mechanotransduction pathway to promote morphogenesis.

Mechanical forces can elicit a mechanotransduction response through junction-associated proteins. In contrast to the wealth of knowledge available for focal adhesions and adherens junctions, much less is known about mechanotransduction at hemidesmosomes. Here, we focus on the plectin homolog VAB-10A, the only evolutionary conserved hemidesmosome component.

Assessing the Contribution of Active and Passive Stresses in C. elegans Elongation.

The role of the actomyosin network is investigated in the elongation of C. elegans during embryonic morphogenesis. We present a model of active elongating matter that combines prestress and passive stress in nonlinear elasticity.

HMP-1/α-catenin promotes junctional mechanical integrity during morphogenesis.

Adherens junctions (AJs) are key structures regulating tissue integrity and maintaining adhesion between cells. During morphogenesis, junctional proteins cooperate closely with the actomyosin network to drive cell movement and shape changes. How the junctions integrate the mechanical forces in space and in time during an in vivo morphogenetic event is still largely unknown, due to a lack of quantitative data.

The apical ECM preserves embryonic integrity and distributes mechanical stress during morphogenesis.

Epithelia are bound by both basal and apical extracellular matrices (ECM). Although the composition and function of the former have been intensively investigated, less is known about the latter. The embryonic sheath, the ECM apical to the embryonic epidermis, has been suggested to promote elongation of the embryo.

The interplay of stiffness and force anisotropies drives embryo elongation.

The morphogenesis of tissues, like the deformation of an object, results from the interplay between their material properties and the mechanical forces exerted on them. The importance of mechanical forces in influencing cell behaviour is widely recognized, whereas the importance of tissue material properties, in particular stiffness, has received much less attention. Using as a model, we examine how both aspects contribute to embryonic elongation.

C. elegans Embryonic Morphogenesis.

Morphogenesis is a four-dimensional process which involves the crucial interplay between signaling, mechanical forces, and spatial changes. Caenorhabditis elegans presents a simple yet versatile model to study morphogenesis. Here, we review recent progress on cellular and molecular drivers of morphological changes during C.