mec-7 is a beta-tubulin gene required for the production of 15-protofilament microtubules in Caenorhabditis elegans.

Directional cell migration is a fundamental process in neural development. In Caenorhabditis elegans , Q neuroblasts on the left (QL) and right (QR) sides of the animal generate cells that migrate in opposite directions along the anteroposterior body axis. The homeobox (Hox) gene lin-39 promotes the anterior migration of QR descendants (QR.x), whereas the canonical Wnt signaling pathway activates another Hox gene, mab-5 , to ensure the QL descendants’ (QL.x) posterior migration. However, the regulatory targets of LIN-39 and MAB-5 remain elusive. Here, we showed that MIG-13, an evolutionarily conserved transmembrane protein, cell-autonomously regulates the asymmetric distribution of the actin cytoskeleton in the leading migratory edge. We identified mig-13 as a cellular target of LIN-39 and MAB-5. LIN-39 establishes QR.x anterior polarity by binding to the mig-13 promoter and promoting mig-13 expression, whereas MAB-5 inhibits QL.x anterior polarity by associating with the lin-39 promoter and downregulating lin-39 and mig-13 expression. Thus, MIG-13 links the Wnt signaling and Hox genes that guide migrations, to the actin cytoskeleton, which executes the motility response in neuronal migration.

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“…S1F and Fig. S2E), Pgcy-32 expresses in Q.ap, Pegl-46 expresses in Q.a/Q.ap and Q.pa/Q.paa, and Pmec-7 expresses in Q.paa (24)(25)(26) (Fig. 2A).…”

Section: Resultsmentioning

confidence: 99%

Transmembrane protein MIG-13 links the Wnt signaling and Hox genes to the cell polarity in neuronal migration

Wang

Zhou

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…mec-7 and mec-12 encode the β-tubulin and α-tubulin subunits of these largediameter microtubules, respectively [29,69]. Mutations in these genes and drugs that depolymerize the specialized microtubules cause animals to become touch insensitive [12,15].…”

Section: Proteins Required For Mechanosensationmentioning

confidence: 99%

Touch sensitivity in Caenorhabditis elegans

Bounoutas

Chalfie

2007

Pflugers Arch - Eur J Physiol

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The nematode Caenorhabditis elegans was the first organism for which touch insensitive mutants were obtained. The study of the genes defective in these mutants has led to the identification of components of a mechanosensory complex needed for specific cells to sense gentle touch to the body. Multiple approaches using genetics, cell biology, biochemistry, and electrophysiology have characterized a channel complex, containing two DEG/ENaC pore-forming subunits and several other proteins, that transduces the touch response. Other mechanical responses, sensed by other cells using a variety of other components, are less well understood in C. elegans. Many of these other senses may use TRP channels, although DEG/ENaC channels have also been implicated.

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“…Mechanosensory neurons have unique large-diameter 15-protofilament microtubules, which are made of cell-specific ␣-MEC-12 and ␤-MEC-7 tubulins (Savage et al, 1989;Fukushige et al, 1999). Worms were grown in the microtubule-depolymerizing drug colchicine, which greatly reduces the microtubule cytoskeleton of only mechanosensory neurons without affecting their neuronal process extension (Chalfie and Thomson, 1982).…”

Section: Misaccumulations Are Microtubule-dependentmentioning

confidence: 99%

Mutations inCaenorhabditis elegansCytoplasmic Dynein Components Reveal Specificity of Neuronal Retrograde Cargo

Koushika

Schaefer²,

Vincent³

et al. 2004

J. Neurosci.

100

113

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We describe Caenorhabditis elegans dynein complex mutants, which misaccumulate synaptic proteins at the ends of neuronal processes. Ultrastructural analysis revealed irregularly sized vesicles that likely represent accumulation of cargo. We propose that synaptobrevin, synaptotagmin, and UNC-104 are specific cargoes of the dynein complex. Many cargoes link to dynein via interactions between dynactin and vesicle-associated spectrin. However, loss of spectrin results in only mild and occasional defects in synaptobrevin localization. Thus, the dynein-dynactin complex shows neuronal cargo selectivity without spectrin being a critical component of cargo binding. We observed parallels to progressive motor neuron disease symptoms in these animals. With age, neuronal misaccumulations increase in size and frequency; locomotion becomes progressively slower; and life span is shortened. These mutants provide a model to assess whether defects in transport of specific cargo mediate neuronal dysfunction.

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mec-7 is a beta-tubulin gene required for the production of 15-protofilament microtubules in Caenorhabditis elegans.

Cited by 295 publications

References 56 publications

Transmembrane protein MIG-13 links the Wnt signaling and Hox genes to the cell polarity in neuronal migration

Transmembrane protein MIG-13 links the Wnt signaling and Hox genes to the cell polarity in neuronal migration

Touch sensitivity in Caenorhabditis elegans

Mutations inCaenorhabditis elegansCytoplasmic Dynein Components Reveal Specificity of Neuronal Retrograde Cargo

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