Asymmetric neural development in theCaenorhabditis elegansolfactory system

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Abstract

Asymmetries in the nervous system have been observed throughout the animal kingdom. Deviations of brain asymmetries are associated with a variety of neurodevelopmental disorders; however, there has been limited progress in determining how normal asymmetry is established in vertebrates. In the Caenorhabditis elegans chemosensory system, two pairs of morphologically symmetrical neurons exhibit molecular and functional asymmetries. This review focuses on the development of antisymmetry of the pair of amphid wing "C" (AWC) olfactory neurons, from transcriptional regulation of general cell identity, establishment of asymmetry through neural network formation and calcium signaling, to the maintenance of asymmetry throughout the life of the animal. Many of the factors that are involved in AWC development have homologs in vertebrates, which may potentially function in the development of vertebrate brain asymmetry.

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Voltage-gated calcium channels.

William Catterall (2011)

Voltage-gated calcium (Ca(2+)) channels are key transducers of membrane potential changes into intracellular Ca(2+) transients that initiate many physiological events. There are ten members of the voltage-gated Ca(2+) channel family in mammals, and they serve distinct roles in cellular signal transduction. The Ca(V)1 subfamily initiates contraction, secretion, regulation of gene expression, integration of synaptic input in neurons, and synaptic transmission at ribbon synapses in specialized sensory cells. The Ca(V)2 subfamily is primarily responsible for initiation of synaptic transmission at fast synapses. The Ca(V)3 subfamily is important for repetitive firing of action potentials in rhythmically firing cells such as cardiac myocytes and thalamic neurons. This article presents the molecular relationships and physiological functions of these Ca(2+) channel proteins and provides information on their molecular, genetic, physiological, and pharmacological properties.

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dSarm/Sarm1 is required for activation of an injury-induced axon death pathway.

J. Osterloh, J Yang, T. M. Rooney … (2012)

Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.

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Stochasticity and cell fate.

Richard Losick, Claude Desplan (2008)

Fundamental to living cells is the capacity to differentiate into subtypes with specialized attributes. Understanding the way cells acquire their fates is a major challenge in developmental biology. How cells adopt a particular fate is usually thought of as being deterministic, and in the large majority of cases it is. That is, cells acquire their fate by virtue of their lineage or their proximity to an inductive signal from another cell. In some cases, however, and in organisms ranging from bacteria to humans, cells choose one or another pathway of differentiation stochastically, without apparent regard to environment or history. Stochasticity has important mechanistic requirements. We speculate on why stochasticity is advantageous-and even critical in some circumstances-to the individual, the colony, or the species.