Calcineurin homologous proteins regulate the membrane localization and activity of sodium/proton exchangers in C. elegans.

Calcineurin B homologous proteins (CHP) are N-myristoylated, EF-hand Ca(2+)-binding proteins that bind to and regulate Na(+)/H(+) exchangers, which occurs through a variety of mechanisms whose relative significance is incompletely understood. Like mammals, Caenorhabditis elegans has three CHP paralogs, but unlike mammals, worms can survive CHP loss-of-function. However, mutants for the CHP ortholog PBO-1 are unfit, and PBO-1 has been shown to be required for proton signaling by the basolateral Na(+)/H(+) exchanger NHX-7 and for proton-coupled intestinal nutrient uptake by the apical Na(+)/H(+) exchanger NHX-2.

miR-786 regulation of a fatty-acid elongase contributes to rhythmic calcium-wave initiation in C. elegans.

Background: Rhythmic behaviors are ubiquitous phenomena in animals. In C. elegans, defecation is an ultradian rhythmic behavior: every ∼50 s a calcium wave initiating in the posterior intestinal cells triggers the defecation motor program that comprises three sequential muscle contractions.

A calcineurin homologous protein is required for sodium-proton exchange events in the C. elegans intestine.

Caenorhabditis elegans defecation is a rhythmic behavior, composed of three sequential muscle contractions, with a 50-s periodicity. The motor program is driven by oscillatory calcium signaling in the intestine. Proton fluxes, which require sodium-proton exchangers at the apical and basolateral intestinal membranes, parallel the intestinal calcium flux.

A calcium wave mediated by gap junctions coordinates a rhythmic behavior in C. elegans.

Intercellular calcium waves can be observed in adult tissues, but whether they are instructive, permissive, or even required for behavior is predominantly unknown. In the nematode Caenorhabditis elegans, a periodic calcium spike in a pacemaker cell initiates a calcium wave in the intestine. The calcium wave is followed by three muscle contractions that comprise the defecation motor program.

Retinoic acid regulates the expression of dorsoventral topographic guidance molecules in the chick retina.

Asymmetric expression of several genes in the early eye anlagen is required for the dorsoventral (DV) and anteroposterior (AP) patterning of the retina. Some of these early patterning genes play a role in determining the graded expression of molecules that are needed to form the retinotectal map. The polarized expression of retinoic acid synthesizing and degrading enzymes along the DV axis in the retina leads to several zones of varied retinoic acid (RA) activity.

The rod photoreceptor pattern is set at the optic vesicle stage and requires spatially restricted cVax expression.

How and when positional identities in the neural retina are established have been addressed primarily with respect to the topographic projections of retinal ganglion cells onto their targets in the brain. Although retinotectal map formation is a prominent manifestation of retinal patterning, it is not the only one. Photoreceptor subtypes are arranged in distinct, species-specific patterns.

The dorsal-ventral axis of the neural retina is divided into multiple domains of restricted gene expression which exhibit features of lineage compartments.

The neural retina is a complex sensory structure designed to receive, integrate, and transmit visual information. An important aspect of retinal development is the establishment of pattern along the dorsal-ventral (D-V) and anterior-posterior (A-P) axes. The recent identification and functional characterization of a dorsal-specific and a ventral-specific transcription factor suggested that the D-V axis is divided into two domains.

Patterning the neural retina.

The early patterning events that shape the neural retina guide the genesis and distribution of postmitotic cell types, as well as their connectivity. The recent discovery of key signaling pathways and transcription factors involved in establishing central, anterior-posterior, and dorsal-ventral retinal patterning has given us insights into the molecular mechanisms controlling these events.