|Feature type||allele||Associated gene||Dmel\Ten-m|
|Also Known As||odzl(3)5309, l(3)05309, Penh22|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Insertion at nucleotide 4191, 30bp from the beginning of transcription.
Insertion in 5' non-coding region of the transcript.
|Caused by insertion|
|Phenotype Manifest In|
Homozygous and Ten-m[CB04632]/Ten-m embryos show defects in the guidance of the intersegmental nerve in the periphery.
Mutant larvae do not have defects in the establishment or maintenance of dendritic tiling in class IV dendrite arborisation (da) neurons.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 1 )|
|Notes on Origin|
The segmentation defects previously reported to be due to the Ten-m mutation are not due to the Ten-m mutation, but instead are caused by a mutation in the opa gene (represented in by the opa[rSS] allele) present on the TM3-rSS balancer in the original stock.
Complements: l(3)0050600506. Complements: Aats-ile00827. Complements: Hem03335. Complements: Csp03988. Complements: l(3)0405304053. Complements: l(3)0907009070. Complements: l(3)04053j8B2. Complements: TyrRneo30.
FlyBase curator comment: FBrf0214744 characterises new loss of function mutations in Ten-m and finds no evidence of a pair-rule segmentation phenotype, in contrast to previous reports. The authors show that the pair-rule phenotype previously reported for a number of Ten-m mutations (including Ten-m) was in fact due to a mutation present on the balancer in the original stock. The segmentation phenotype described in FBrf0075161, FBrf0073721, FBrf0098973 and FBrf0204395 for Ten-m has thus been removed from the allele report in FlyBase, since it is not due to the mutation in Ten-m.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 10 )|
|Secondary FlyBase IDs|
|References ( 18 )|
|Personal communication to FlyBase|