|Feature type||allele||Associated gene||Dmel\trpm|
|Also Known As||dTRPM28|
|Allele class||amorphic allele - genetic evidence, hypomorphic allele - molecular evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
Mutant animals show prolonged larval development, at the end of which they arrest and die at the prepupal stage. The mutant larvae have a lower body weight compared to controls throughout larval development, with the difference in weight being greatest at the end of the second larval instar. Mutant animals lacking both maternal and zygotic function show an obvious growth defect by the end of the first larval instar, weighing less than controls. This defect progresses rapidly so that by the middle of the second instar they are approximately 17% the weight of controls. These larvae die approximately 48 hours after hatching. The growth defect seen in mutant animals is underpinned by a reduction in cell size, whereas cell numbers and DNA replication are normal. Mitochondria in mutant salivary glands are fused to form long tubular structures (in wild type they are seen as individual bullet-shaped structures).
Homozygotes die at the end of the larval stage, at the point of white prepupae formation.
|Phenotype Manifest In|
trpm28 is a suppressor of embryonic/larval salivary gland phenotype of Pi3K92EScer\UAS.T:Hsap\MYC, Scer\GAL4AB1
Expression of Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[AB1] in a trpm background does not result in an increase in cell size in the larval salivary gland. Expression of S6k[STDETE.Scer\UAS] under the control of Scer\GAL4[AB1] in a trpm background does not result in an increase in cell size in the salivary gland.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 2 )|