mec-15 encodes an F-box protein with WD repeats required for proper touch receptor neuron mechanosensation, morphology, and synapse development. Export

@inproceedings{citeulike:3333218, abstract = { The mec-15 gene was originally identified in a screen for touch insensitive mutants. mec-15 mutations cause partial touch insensitivity that is temperature sensitive. The sam-3 mutation was identified in an independent screen for animals with mislocalized presynaptic markers in the touch receptor neurons; this phenotype is also temperature sensitive. mec-15 and sam-3 are the same gene, since mec-15 and sam-3 alleles fail to complement each other for partial touch insensitivity and presynaptic marker mislocalization. All alleles also affect touch receptor neuron morphology, causing an enlargement of the cell body. We used Snip-SNP mapping and gene sequencing to identify T01E8.4 as mec-15/sam-3. T01E8.4 encodes a 406 a.a. protein containing an F-box domain and WD repeats. Interestingly, F-box proteins, which act as protein substrate adaptors in ubiquitin ligase complexes, have been implicated in C. elegans ventral cord synapse formation (Liao et al. Nature 430: 345-350, 2004). All mec-15/sam-3 alleles save one are nonsense mutations in the T01E8.4 coding sequence; the remaining allele has two missense mutations. The mutant alleles in trans to a deletion of the region do not produce an enhanced phenotype, suggesting that the alleles are functional nulls. Transforming mec-15 mutants with the T01E8.4 gene rescues their mechanosensitive abnormal phenotype. The protein-GFP fusion is expressed in several neurons including the touch receptor neurons, where its expression is cytoplasmic, absent in adults, and dependent on the MEC-3 transcription factor. We are examining gene interactions to identify proteins that are needed for mec-15 action. Since a p38 MAP kinase pathway has been implicated in ventral cord synapse development (Nakata et al. Cell 120: 407-420, 2005), we examined mec-15 phenotypes in a pmk-3 background; all the phenotypes were enhanced. In addition, loss of one copy of the mec-7 <font face=symbol>b</font>-tubulin gene suppresses mec-15 phenotypes, suggesting an interaction between MEC-15 and the touch receptor neurons'' specialized microtubules.}, author = {Bounoutas, Alexander and Zheng, Kun and Nonet, Michael L. and Chalfie, Martin}, citeulike-article-id = {3333218}, citeulike-linkout-0 = {http://www.wormbase.org/db/misc/paper?name=WBPaper00030335}, journal = {International Worm Meeting}, keywords = {c\_elegans, caenorhabditis\_elegans, celegans, elegans, f42g84, mec-15, mec-7, meeting\_abstract, nematode, pmk-3, wormbase, zk1543}, posted-at = {2008-09-24 18:40:56}, priority = {3}, title = {mec-15 encodes an F-box protein with WD repeats required for proper touch receptor neuron mechanosensation, morphology, and synapse development.}, url = {http://www.wormbase.org/db/misc/paper?name=WBPaper00030335}, year = {2007} }

TY - CONF ID - citeulike:3333218 L3 - citeulike-article-id:3333218 N2 - The mec-15 gene was originally identified in a screen for touch insensitive mutants. mec-15 mutations cause partial touch insensitivity that is temperature sensitive. The sam-3 mutation was identified in an independent screen for animals with mislocalized presynaptic markers in the touch receptor neurons; this phenotype is also temperature sensitive. mec-15 and sam-3 are the same gene, since mec-15 and sam-3 alleles fail to complement each other for partial touch insensitivity and presynaptic marker mislocalization. All alleles also affect touch receptor neuron morphology, causing an enlargement of the cell body. We used Snip-SNP mapping and gene sequencing to identify T01E8.4 as mec-15/sam-3. T01E8.4 encodes a 406 a.a. protein containing an F-box domain and WD repeats. Interestingly, F-box proteins, which act as protein substrate adaptors in ubiquitin ligase complexes, have been implicated in C. elegans ventral cord synapse formation (Liao et al. Nature 430: 345-350, 2004). All mec-15/sam-3 alleles save one are nonsense mutations in the T01E8.4 coding sequence; the remaining allele has two missense mutations. The mutant alleles in trans to a deletion of the region do not produce an enhanced phenotype, suggesting that the alleles are functional nulls. Transforming mec-15 mutants with the T01E8.4 gene rescues their mechanosensitive abnormal phenotype. The protein-GFP fusion is expressed in several neurons including the touch receptor neurons, where its expression is cytoplasmic, absent in adults, and dependent on the MEC-3 transcription factor. We are examining gene interactions to identify proteins that are needed for mec-15 action. Since a p38 MAP kinase pathway has been implicated in ventral cord synapse development (Nakata et al. Cell 120: 407-420, 2005), we examined mec-15 phenotypes in a pmk-3 background; all the phenotypes were enhanced. In addition, loss of one copy of the mec-7 <font face=symbol>b</font>-tubulin gene suppresses mec-15 phenotypes, suggesting an interaction between MEC-15 and the touch receptor neurons'' specialized microtubules. JF - International Worm Meeting TI - mec-15 encodes an F-box protein with WD repeats required for proper touch receptor neuron mechanosensation, morphology, and synapse development. KW - c_elegans KW - caenorhabditis_elegans KW - celegans KW - elegans KW - f42g84 KW - mec-15 KW - mec-7 KW - meeting_abstract KW - nematode KW - pmk-3 KW - wormbase KW - zk1543 AU - Bounoutas, Alexander AU - Zheng, Kun AU - Nonet, Michael AU - Chalfie, Martin PY - 2007/// UR - http://www.wormbase.org/db/misc/paper?name=WBPaper00030335 ER -