Developmental plasticity: a worm's eye view.

Numerous examples of different phenotypic outcomes in response to varying environmental conditions have been described across phyla, from plants to mammals. Here, we examine the impact of the environment on different developmental traits, focusing in particular on one key environmental variable, nutrient availability. We present advances in our understanding of developmental plasticity in response to food variation using the nematode Caenorhabditis elegans, which provides a near-isogenic context while permitting lab-controlled environments and analysis of wild isolates.

A natural transdifferentiation event involving mitosis is empowered by integrating signaling inputs with conserved plasticity factors.

Transdifferentiation, or direct cell reprogramming, is the conversion of one fully differentiated cell type into another. Whether core mechanisms are shared between natural transdifferentiation events when occurring with or without cell division is unclear. We have previously characterized the Y-to-PDA natural transdifferentiation in Caenorhabditis elegans, which occurs without cell division and requires orthologs of vertebrate reprogramming factors.

Publisher Correction: An actin-based viscoplastic lock ensures progressive body-axis elongation.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

Publisher Correction: An actin-based viscoplastic lock ensures progressive body-axis elongation.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

An actin-based viscoplastic lock ensures progressive body-axis elongation.

Body-axis elongation constitutes a key step in animal development, laying out the final form of the entire animal. It relies on the interplay between intrinsic forces generated by molecular motors, extrinsic forces exerted by adjacent cells and mechanical resistance forces due to tissue elasticity or friction. Understanding how mechanical forces influence morphogenesis at the cellular and molecular level remains a challenge.

Noncentrosomal microtubules in C. elegans epithelia.

The microtubule cytoskeleton has a dual contribution to cell organization. First, microtubules help displace chromosomes and provide tracks for organelle transport. Second, microtubule rigidity confers specific mechanical properties to cells, which are crucial in cilia or mechanosensory structures.

Functional and Genetic Analysis of VAB-10 Spectraplakin in Caenorhabditis elegans.

Intermediate filaments (IFs) are involved in multiple cellular processes that are essential for the maintenance of cell and tissue integrity. To achieve this crucial function, IFs have to be organized as long and resistant filaments across the cells and to be tightly anchored at the cell periphery. This anchoring takes place at the level desmosomes and hemidesmosomes through proteins belonging to the spectraplakin family.

Non-centrosomal epidermal microtubules act in parallel to LET-502/ROCK to promote C. elegans elongation.

C. elegans embryonic elongation is a morphogenetic event driven by actomyosin contractility and muscle-induced tension transmitted through hemidesmosomes. A role for the microtubule cytoskeleton has also been proposed, but its contribution remains poorly characterized.

MIG-15 and ERM-1 promote growth cone directional migration in parallel to UNC-116 and WVE-1.

Neurons require precise targeting of their axons to form a connected network and a functional nervous system. Although many guidance receptors have been identified, much less is known about how these receptors signal to direct growth cone migration. We used Caenorhabditis elegans motoneurons to study growth cone directional migration in response to a repellent UNC-6 (netrin homolog) guidance cue.

Tissue morphogenesis: how multiple cells cooperate to generate a tissue.

Genetic analysis in model organisms has recently achieved a detailed molecular description of many key cellular processes controlling embryonic morphogenesis. To understand higher order tissue morphogenesis, we now need to define how these processes become integrated across different cell groups and cell layers. Here, we review progress in this fast moving area, which was to a large degree made possible by novel imaging methods and the increasingly frequent use of modeling.

Myosin II regulation during C. elegans embryonic elongation: LET-502/ROCK, MRCK-1 and PAK-1, three kinases with different roles.

Myosin II plays a central role in epithelial morphogenesis; however, its role has mainly been examined in processes involving a single cell type. Here we analyze the structure, spatial requirement and regulation of myosin II during C. elegans embryonic elongation, a process that involves distinct epidermal cells and muscles.

The WAVE/SCAR complex promotes polarized cell movements and actin enrichment in epithelia during C. elegans embryogenesis.

The WAVE/SCAR complex promotes actin nucleation through the Arp2/3 complex, in response to Rac signaling. We show that loss of WVE-1/GEX-1, the only C. elegans WAVE/SCAR homolog, by genetic mutation or by RNAi, has the same phenotype as loss of GEX-2/Sra1/p140/PIR121, GEX-3/NAP1/HEM2/KETTE, or ABI-1/ABI, the three other components of the C.

Epithelial morphogenesis in embryos: asymmetries, motors and brakes.

Epithelial cells play a central role in many embryonic morphogenetic processes, during which they undergo highly coordinated cell shape changes. Here, we review some common principles that have recently emerged through genetic and cellular analyses performed mainly with invertebrate genetic models, focusing on morphogenetic processes involving epithelial sheets. All available data argue that myosin II is the main motor that induces cell shape changes during morphogenesis.

A transmembrane protein required for acetylcholine receptor clustering in Caenorhabditis elegans.

Clustering neurotransmitter receptors at the synapse is crucial for efficient neurotransmission. Here we identify a Caenorhabditis elegans locus, lev-10, required for postsynaptic aggregation of ionotropic acetylcholine receptors (AChRs). lev-10 mutants were identified on the basis of weak resistance to the anthelminthic drug levamisole, a nematode-specific cholinergic agonist that activates AChRs present at neuromuscular junctions (NMJs) resulting in muscle hypercontraction and death at high concentrations.

[C. elegans: of neurons and genes].

The human brain contains 100 billion neurons and probably one thousand times more synapses. Such a system can be analyzed at different complexity levels, from cognitive functions to molecular structure of ion channels. However, it remains extremely difficult to establish links between these different levels.

Telomeric associated sequences of Drosophila recruit polycomb-group proteins in vivo and can induce pairing-sensitive repression.

In Drosophila, relocation of a euchromatic gene near centromeric or telomeric heterochromatin often leads to its mosaic silencing. Nevertheless, modifiers of centromeric silencing do not affect telomeric silencing, suggesting that each location requires specific factors. Previous studies suggest that a subset of Polycomb-group (PcG) proteins could be responsible for telomeric silencing.

GABA is dispensable for the formation of junctional GABA receptor clusters in Caenorhabditis elegans.

At GABAergic synapses, GABA receptors form high-density clusters opposite GABA release sites. Whether GABA release per se plays a role in the formation of GABA receptor clusters remains uncertain. To address this question in vivo, we characterized GABA receptor clustering in the nematode Caenorhabditis elegans.