Allele Dmel\SNF1A³

General Information
Symbol	Dmel\SNF1A³	Species	D. melanogaster
Name		FlyBase ID	FBal0241421
Feature type	allele	Associated gene	Dmel\SNF1A
Also Known As	ampkα³

Allele class	amorphic allele - genetic evidence
Mutagen	ethyl methanesulfonate
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Mirouse et al., 2007)
Mutagen	ethyl methanesulfonate (Mirouse et al., 2007)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: Y141@. (Mirouse et al., 2007)
Cytology
Phenotypic Data
Phenotypic Class
	immune response defective \| dominant (Chakrabarti et al., 2012) lethal \| larval stage (Johnson et al., 2010) lethal \| recessive \| second instar larval stage (Mirouse et al., 2007) neuroanatomy defective (Mirouse et al., 2007, Kazgan et al., 2010) small body (Johnson et al., 2010) starvation stress response defective (Johnson et al., 2010)
Phenotype Manifest In
	class IV dendritic arborizing neuron (Johnson et al., 2010) follicle cell \| somatic clone (Mirouse et al., 2007) oenocyte (Johnson et al., 2010) plasma membrane & dendrite (Mirouse et al., 2007) sensory neuron (Kazgan et al., 2010) stress fiber & follicle cell \| somatic clone (Mirouse et al., 2007)
Detailed Description
	Statement Reference Heterozygous flies are more resistant to P. entomophila infection than control flies. (Chakrabarti et al., 2012) SNF1A[3] mutants exhibit aberrant morphology in class IV multi-dendritic neurons. SNF1A[3] mutants die as larvae and are characteristically smaller than wild-type larvae of the same age. The majority of SNF1A[3] 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[3] larvae show significantly more and larger lipid droplets in oenocytes compared to controls, resembling the starved phenotype of wild-type oenocytes. (Johnson et al., 2010) 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[3] follicle cell clones show normal epithelial polarity. Under energetic stress conditions, SNF1A[3] 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. (Mirouse et al., 2007)
External Data
Linkouts
Interactions
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	SNF1A³ is rescued by Scer\GAL4^109(2)80/SNF1A^Scer\UAS.cMa (Mirouse et al., 2007, Kazgan et al., 2010) SNF1A³ is rescued by Scer\GAL4^Ubi/SNF1A^{Scer\UAS.T:Disc\RFP-mCherry} (Mirouse et al., 2007)
Not rescued by	SNF1A³ is not rescued by Scer\GAL4^109(2)80/SNF1A^ΔC.Scer\UAS (Kazgan et al., 2010)
Comments	Expression of SNF1A[Scer\UAS.cMa] under the control of Scer\GAL4[109(2)80] rescues the neuronal defects of SNF1A[3] mutants. Expression of SNF1A[ΔC.Scer\UAS] under the control of Scer\GAL4[109(2)80] fails to rescue the neuronal defects of SNF1A[3] mutants. (Kazgan et al., 2010)
Stocks ( 1 )
Bloomington	33831 SNF1A³/FM7i
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	AMPK³ (Johnson et al., 2010) ampkα³ (Mirouse et al., 2007, Chakrabarti et al., 2012) AMPKα³ (Kazgan et al., 2010) SNF1A³
Name Synonym
Secondary FlyBase IDs

References ( 4 )
Research paper	Chakrabarti et al., 2012, Cell Host Microbe 12(1): 60--70 Infection-induced host translational blockage inhibits immune responses and epithelial renewal in the Drosophila gut. [FBrf0218984] Johnson et al., 2010, PLoS ONE 5(9): e12799 Altered metabolism and persistent starvation behaviors caused by reduced AMPK function in Drosophila. [FBrf0211905] Kazgan et al., 2010, Mol. Biol. Cell 21(19): 3433--3442 Identification of a nuclear export signal in the catalytic subunit of AMP-activated protein kinase. [FBrf0211940] Mirouse et al., 2007, J. Cell Biol. 177(3): 387--392 LKB1 and AMPK maintain epithelial cell polarity under energetic stress. [FBrf0201625]

Allele Dmel\SNF1A3

Allele Dmel\SNF1A³