Dmel\P{SUPor-P}Atg18^KG03090 Insertion

General Information
Symbol	Dmel\P{SUPor-P}Atg18^KG03090	Species	D. melanogaster
Name		FlyBase ID	FBti0023117
Feature type	transposable_element_insertion_site
Description
Inserted element	P{SUPor-P}	Expression data
Affected gene(s)	Atg18	Viability / fertility
Causes allele(s)	Atg18^KG03090	Stock availability	1 publicly available
LINE ID	KG03090
Genomic Location
Chromosomal location	3L ( 66B11 )	Sequence location	3L:8,180,476..8,180,476 [-]
Map ( GBrowse )
Member of Large Scale Dataset(s)
Dataset	TI_set_P{SUPor-P}.KG A set of transgenic insertion stocks derived by TE mobilization using the P-element construct P{SUPor-P}; created and vetted by the Gene Disruption Project (GDP). The P{SUPor-P} construct carries two visible markers: a w[+mC] mini-white marker flanked by su(Hw)-binding sites, designed to reduce the variablity of the phenotype of the white gene marker due position effects, in addition to the mini-yellow marker y[+mDint2]. (Bellen et al., 2004)
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
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Detailed Mapping Data
Chromosome (arm)
Sequence Location	3L:8,180,476..8,180,476 [-] (Gene Disruption Project members, 2001-)
Orientation
Cytological location (computed by FlyBase)	66B11 ( inferred by FlyBase from sequence location )
Cytological location (reported)	66B13 (reported as inferred from sequence location) (Gene Disruption Project members, 2001-)
Comments concerning location
Sequence Data
Flanking sequence	BH809427 (Gene Disruption Project members, 2001-, FlyBase, 1992-)
Inserted Element
Construct	P{SUPor-P}
Location-dependent role
Size	11.467Kb
Associated alleles	gypsy\su(Hw)BR⁴³⁰ w^BR.E.BR y^+mDint2
Molecular map
Affected Gene(s)
Insertion may affect gene	Atg18 (Gene Disruption Project members, 2001-, Tian et al., 2011, Shen and Ganetzky, 2009, Pircs et al., 2012)
Alleles and Phenotypes
Causes alleles	Atg18^KG03090 (Gene Disruption Project members, 2001-, Scott et al., 2004, Tian et al., 2011, Shen and Ganetzky, 2009, Pircs et al., 2012)

Lethality References lethal \| larval stage \| recessive (Scott et al., 2004)
Sterility References
Phenotype Manifest In
	embryonic/larval fat body \| third instar larval stage (Pircs et al., 2012) embryonic/larval midgut \| P-stage (Denton et al., 2009) embryonic/larval salivary gland (Berry and Baehrecke, 2007) NMJ bouton (Shen and Ganetzky, 2009)
Detailed Description
Statement Reference Atg18[KG03090] mutants display basal autophagy defects in larval fat body cells. (Pircs et al., 2012) Atg18[KG03090] heterozygous neuromuscular junctions exhibit wild-type bouton levels. (Tian et al., 2011) An Atg18[KG03090] heterozygous background dominantly suppresses the increase in bouton number seen in Rae1[EX28] homozygous mutant neuromuscular junction. (Tian et al., 2011) Atg18[KG03090]/Df(3L)Exel6112 animals analysed at +4 hours relative to puparium formation show a significant delay in midgut histolysis compared to controls. At +12 hours relative to puparium formation, larval midgut contraction is dramatically delayed in the mutants compared to controls. (Denton et al., 2009) Larvae homozygous for Atg18[KG03090] show abnormal autophagic response to starvation. (Köhler et al., 2009) Atg18[KG03090]/+ mutants exhibit a neuromuscular junction undergrowth phenotype but do not exhibit defects in axonal transport. (Shen and Ganetzky, 2009) At 24 hours after puparium formation, Atg18^KG03090/Df(3L)66C-G28 animals expressing still contain vacuolated salivary gland fragments, in contrast to wild-type animals, where the salivary glands have completely degraded by this stage. DNA fragmentation is detected by TUNEL in salivary glands of Atg18^KG03090/Df(3L)Exel6112 animals at 13.5 hours after puparium formation, as occurs in control salivary glands at this stage. (Berry and Baehrecke, 2007) Mutants show disruption of autophagy. (Scott et al., 2004)
Expression Data
Reporter Expression

Additional Information
Statement Reference

Marker for
Reflects expression of
Reporter construct used in assay
External Images
FlyView (LinkOut)
Data on Genetic Line
Line ID	KG03090 (Gene Disruption Project members, 2001-)
Origin as a multiple insertion line
Progenitor(s) within the Genome

Related Aberration or Balancer
Aberration
Balancer
Stocks ( 1 )
Bloomington	13945 y¹; P{SUPor-P}Atg18^KG03090 ry⁵⁰⁶/TM3, Sb¹ Ser¹
Linkouts
Comments
	Location 3L:8161323-8161324 confirmed by FlyBase alignment of dbGSS accession BH809427 to D. melanogaster arm Release_4 and heterochromatin Release_3.2b. Insertion orientation revised. (FlyBase, 2005)
Synonyms & Secondary IDs
Reported As
Symbol Synonym	Atg18^KG03090 (Tian et al., 2011) atg18^KG03090 (Shen and Ganetzky, 2009) Atg18a^KG03090 (Pircs et al., 2012) KG03090 (Gene Disruption Project members, 2001-, FlyBase, 1992-) P{SUPor-P}Atg18^KG03090 (FlyBase, 2005, FlyBase, 1992-, ) P{SUPor-P}CG7986^KG03090 (FlyBase, 1992-)
Secondary FlyBase IDs

References ( 12 )
Research paper	Pircs et al., 2012, PLoS ONE 7(8): e44214 Advantages and Limitations of Different p62-Based Assays for Estimating Autophagic Activity in Drosophila. [FBrf0219364] Tian et al., 2011, Nat. Neurosci. 14(10): 1267--1275 Drosophila Rae1 controls the abundance of the ubiquitin ligase Highwire in post-mitotic neurons. [FBrf0216253] Denton et al., 2009, Curr. Biol. 19(20): 1741--1746 Autophagy, not apoptosis, is essential for midgut cell death in Drosophila. [FBrf0209243] Köhler et al., 2009, Autophagy 5(7): 980--990 A combined proteomic and genetic analysis identifies a role for the lipid desaturase Desat1 in starvation-induced autophagy in Drosophila. [FBrf0208992] Shen and Ganetzky, 2009, J. Cell Biol. 187(1): 71--79 Autophagy promotes synapse development in Drosophila. [FBrf0208921] Berry and Baehrecke, 2007, Cell 131(6): 1137--1148 Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila. [FBrf0200408] Bellen et al., 2004, Genetics 167(2): 761--781 The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132]
Supplementary material	Scott et al., 2004, Dev. Cell 7(2): Supplementary material. [FBrf0183440]
Personal communication to FlyBase	Gene Disruption Project members, 2001-, (Computer file) (Computer file) [FBrf0132177]
FlyBase analysis	FlyBase Curators, 2013, Members of GDP insertion collections: P{GT1}, P{SUPor-P}, P{EPgy2}, Mi{ET1}, Mi{MIC}. Members of GDP insertion collections: P{GT1}, P{SUPor-P}, P{EPgy2}, Mi{ET1}, Mi{MIC}. [FBrf0220667] FlyBase, 2005, Assessment of transgenic construct insertion sites. Assessment of transgenic construct insertion sites. [FBrf0184339] FlyBase, 1992-, FlyBase curation. FlyBase curation. [FBrf0105495]

Dmel\P{SUPor-P}Atg18KG03090 Insertion

Dmel\P{SUPor-P}Atg18^KG03090 Insertion