|Feature type||allele||Associated gene||Dmel\SNF1A|
|Also Known As||ampkα3|
|Allele class||amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: Y141@.
|Phenotype Manifest In|
plasma membrane & dendrite
stress fiber & follicle cell | somatic clone
Heterozygous flies are more resistant to P. entomophila infection than control flies.
SNF1A mutants exhibit aberrant morphology in class IV multi-dendritic neurons. SNF1A mutants die as larvae and are characteristically smaller than wild-type larvae of the same age. The majority of SNF1A mutants die between the fifth and seventh day of the third instar larval stage. Feeding these larvae with Rapamycin increases the percentage of mutant larvae surviving to the seventh day. Under fed conditions, SNF1A larvae show significantly more and larger lipid droplets in oenocytes compared to controls, resembling the starved phenotype of wild-type oenocytes.
Homozygotes have enlarged plasma membrane domains in sensory neuron dendrites, but not in axonal compartments. Actin defects are not seen in homozygous follicle cell clones in females raised under normal food conditions. However, under energetic stress conditions (strongly reducing the availability of sugar in the food medium), 98% of homozygous follicle cell clones show a strong mutant actin phenotype; the density of the basal stress fibres is strongly reduced, whereas the amount of apical F-actin increases. Under normal food conditions, SNF1A follicle cell clones show normal epithelial polarity. Under energetic stress conditions, SNF1A follicle cell clones show a fully penetrant loss of epithelial polarity. Many of the clones show a severe phenotype, in which the cells round up and lose their epithelial organisation to form multiple layers of cells. Larger mutant clones, particularly those at the anterior or posterior of the egg chamber, show a complete loss of epithelial organisation and overproliferate to form small, tumour-like growths of unpolarised cells. Homozygous follicle cell clones do not show polarity defects in females fed on a glucose-only diet.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
|Secondary FlyBase IDs|
|References ( 4 )|