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Extension of the Caenorhabditis elegans Pharyngeal M1 neuron axon is regulated by multiple mechanisms.

Refai O, Rohs P, Mains PE, Gaudet J - G3 (Bethesda) (2013)

Bottom Line: We found that extension of the M1 pharyngeal axon, which spans the entire length of the pharynx, occurs in two distinct phases.The first proximal phase does not require genes that function in axon extension (unc-34, unc-51, unc-115, and unc-119), whereas the second distal phase does use these genes and is guided in part by the adjacent g1P gland cell projection. unc-34, unc-51, and unc-115 had incompletely penetrant defects and appeared to act in conjunction with the g1P cell for distal outgrowth.One of these mutations appeared to affect the generation or differentiation of the M1 neuron.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alberta T2N 4N1, Canada.

ABSTRACT
The guidance of axons to their correct targets is a critical step in development. The C. elegans pharynx presents an attractive system to study neuronal pathfinding in the context of a developing organ. The worm pharynx contains relatively few cells and cell types, but each cell has a known lineage and stereotyped developmental patterns. We found that extension of the M1 pharyngeal axon, which spans the entire length of the pharynx, occurs in two distinct phases. The first proximal phase does not require genes that function in axon extension (unc-34, unc-51, unc-115, and unc-119), whereas the second distal phase does use these genes and is guided in part by the adjacent g1P gland cell projection. unc-34, unc-51, and unc-115 had incompletely penetrant defects and appeared to act in conjunction with the g1P cell for distal outgrowth. Only unc-119 showed fully penetrant defects for the distal phase. Mutations affecting classical neuronal guidance cues (Netrin, Semaphorin, Slit/Robo, Ephrin) or adhesion molecules (cadherin, IgCAM) had, at best, weak effects on the M1 axon. None of the mutations we tested affected the proximal phase of M1 elongation. In a forward genetic screen, we isolated nine mutations in five genes, three of which are novel, showing defects in M1, including axon overextension, truncation, or ectopic branching. One of these mutations appeared to affect the generation or differentiation of the M1 neuron. We conclude that M1 axon extension is a robust process that is not completely dependent on any single guidance mechanism.

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Model for M1 axon guidance. M1 is shown in green and g1P is shown in red. M1 development is divided into two steps. During phase 1, M1 builds its proximal trajectory independent of genes affecting growth cones. In phase 2, M1 builds its distal trajectory, which is affected in growth cone–defective mutants and loss of the g1P cell. The regions where M1 axon phenotypes occur are shown for each gene. These genes are categorized in groups, which act in metacorpus, procorpus, and or at the anterior pharyngeal tip, where the axon terminates. The unc-119 (which also acts for distal extension), mnm-7, and vab-1 are necessary for preventing ectopic branching in the isthmus or terminal bulb, rather than axon extension in those regions.
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fig8: Model for M1 axon guidance. M1 is shown in green and g1P is shown in red. M1 development is divided into two steps. During phase 1, M1 builds its proximal trajectory independent of genes affecting growth cones. In phase 2, M1 builds its distal trajectory, which is affected in growth cone–defective mutants and loss of the g1P cell. The regions where M1 axon phenotypes occur are shown for each gene. These genes are categorized in groups, which act in metacorpus, procorpus, and or at the anterior pharyngeal tip, where the axon terminates. The unc-119 (which also acts for distal extension), mnm-7, and vab-1 are necessary for preventing ectopic branching in the isthmus or terminal bulb, rather than axon extension in those regions.

Mentions: We demonstrated that the extension of the M1 axon occurs in two distinct phases (Figure 8). The first (proximal) phase through the isthmus was normal under all of the conditions we tested and not affected by gland ablation, mutations that impair growth cone function, axonal outgrowth, or mutations in genes known to affect axon guidance or cell adhesion. Moreover, none of the mutants that we isolated from our screen for M1 defects exhibited abnormalities during the proximal phase of axon extension. In contrast, the subsequent distal phase of M1 axon extension through the metacorpus and procorpus was often abnormal after gland ablation, with mutations affecting growth cones and axonal outgrowth, and, to a lesser extent, with mutations affecting axon guidance.


Extension of the Caenorhabditis elegans Pharyngeal M1 neuron axon is regulated by multiple mechanisms.

Refai O, Rohs P, Mains PE, Gaudet J - G3 (Bethesda) (2013)

Model for M1 axon guidance. M1 is shown in green and g1P is shown in red. M1 development is divided into two steps. During phase 1, M1 builds its proximal trajectory independent of genes affecting growth cones. In phase 2, M1 builds its distal trajectory, which is affected in growth cone–defective mutants and loss of the g1P cell. The regions where M1 axon phenotypes occur are shown for each gene. These genes are categorized in groups, which act in metacorpus, procorpus, and or at the anterior pharyngeal tip, where the axon terminates. The unc-119 (which also acts for distal extension), mnm-7, and vab-1 are necessary for preventing ectopic branching in the isthmus or terminal bulb, rather than axon extension in those regions.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3815062&req=5

fig8: Model for M1 axon guidance. M1 is shown in green and g1P is shown in red. M1 development is divided into two steps. During phase 1, M1 builds its proximal trajectory independent of genes affecting growth cones. In phase 2, M1 builds its distal trajectory, which is affected in growth cone–defective mutants and loss of the g1P cell. The regions where M1 axon phenotypes occur are shown for each gene. These genes are categorized in groups, which act in metacorpus, procorpus, and or at the anterior pharyngeal tip, where the axon terminates. The unc-119 (which also acts for distal extension), mnm-7, and vab-1 are necessary for preventing ectopic branching in the isthmus or terminal bulb, rather than axon extension in those regions.
Mentions: We demonstrated that the extension of the M1 axon occurs in two distinct phases (Figure 8). The first (proximal) phase through the isthmus was normal under all of the conditions we tested and not affected by gland ablation, mutations that impair growth cone function, axonal outgrowth, or mutations in genes known to affect axon guidance or cell adhesion. Moreover, none of the mutants that we isolated from our screen for M1 defects exhibited abnormalities during the proximal phase of axon extension. In contrast, the subsequent distal phase of M1 axon extension through the metacorpus and procorpus was often abnormal after gland ablation, with mutations affecting growth cones and axonal outgrowth, and, to a lesser extent, with mutations affecting axon guidance.

Bottom Line: We found that extension of the M1 pharyngeal axon, which spans the entire length of the pharynx, occurs in two distinct phases.The first proximal phase does not require genes that function in axon extension (unc-34, unc-51, unc-115, and unc-119), whereas the second distal phase does use these genes and is guided in part by the adjacent g1P gland cell projection. unc-34, unc-51, and unc-115 had incompletely penetrant defects and appeared to act in conjunction with the g1P cell for distal outgrowth.One of these mutations appeared to affect the generation or differentiation of the M1 neuron.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alberta T2N 4N1, Canada.

ABSTRACT
The guidance of axons to their correct targets is a critical step in development. The C. elegans pharynx presents an attractive system to study neuronal pathfinding in the context of a developing organ. The worm pharynx contains relatively few cells and cell types, but each cell has a known lineage and stereotyped developmental patterns. We found that extension of the M1 pharyngeal axon, which spans the entire length of the pharynx, occurs in two distinct phases. The first proximal phase does not require genes that function in axon extension (unc-34, unc-51, unc-115, and unc-119), whereas the second distal phase does use these genes and is guided in part by the adjacent g1P gland cell projection. unc-34, unc-51, and unc-115 had incompletely penetrant defects and appeared to act in conjunction with the g1P cell for distal outgrowth. Only unc-119 showed fully penetrant defects for the distal phase. Mutations affecting classical neuronal guidance cues (Netrin, Semaphorin, Slit/Robo, Ephrin) or adhesion molecules (cadherin, IgCAM) had, at best, weak effects on the M1 axon. None of the mutations we tested affected the proximal phase of M1 elongation. In a forward genetic screen, we isolated nine mutations in five genes, three of which are novel, showing defects in M1, including axon overextension, truncation, or ectopic branching. One of these mutations appeared to affect the generation or differentiation of the M1 neuron. We conclude that M1 axon extension is a robust process that is not completely dependent on any single guidance mechanism.

Show MeSH
Related in: MedlinePlus