Allele Dmel\armi^72.1

General Information
Symbol	Dmel\armi^72.1	Species	D. melanogaster
Name		FlyBase ID	FBal0155636
Feature type	allele	Associated gene	Dmel\armi

Allele class	loss of function allele
Mutagen	Delta2-3
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.
Nature of the Allele
Allele class	loss of function allele (Cook et al., 2004)
Mutagen	Delta2-3 (Cook et al., 2004)
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	armi¹ (Cook et al., 2004, Tomari et al., 2004)
Nature of the lesion	Statement Reference Imprecise excision of the P-element, resulting in a deletion of armi sequences in the 5' untranslated region. (Tomari et al., 2004)
Cytology
Phenotypic Data
Phenotypic Class
	female sterile (Cook et al., 2004) lethal \| embryonic stage \| maternal effect (with armi¹) (Orsi et al., 2010) male sterile \| partially (Tomari et al., 2004) memory defective (with Df(3L)E1) (Ashraf et al., 2006) memory defective \| recessive (Ashraf et al., 2006)
Phenotype Manifest In
	dorsal appendage (with armi¹) (Klattenhoff et al., 2007, Orsi et al., 2010) dorsal appendage \| maternal effect (Cook et al., 2004, Tomari et al., 2004) dorsal appendage \| maternal effect (with armi¹) (Klattenhoff et al., 2009) egg \| maternal effect (Cook et al., 2004) microtubule organizing center & oocyte (with armi¹) (Klattenhoff et al., 2007) oocyte & microtubule (Cook et al., 2004) oocyte & microtubule organizing center (Cook et al., 2004)
Detailed Description
	Statement Reference Eggs laid by armi[1]/armi[72.1] females have dorsal appendage defects; 11.7% have fused dorsal appendages, 88.1% lack dorsal appendages and 0.2% have wild-type dorsal appendages. (Orsi et al., 2010) Only 2% of eggs derived from armi[1]/armi[72.1] females have two wild-type dorsal appendages, compared with 11% if the females are fed caffeine. (Klattenhoff et al., 2009) armi^72.1/armi¹ eggs show fused appendages in 67.6% of cases, no appendages in 28.9% of cases and the wild-type number of appendages in 3.5% of cases. In armi^72.1/armi¹ oocytes, both the anterior and later posterior microtubule-organizing centers are much less prominent than in wild-type oocytes. (Klattenhoff et al., 2007) armi^72.1 and armi^72.1/Df(3L)E1 flies have a deficient long-term olfactory memory but show no defects in short-term olfactory memory. (Ashraf et al., 2006) 92% of eggs laid by armi^72.1 females completely lack dorsal appendages (indicating strong dorsal/ventral patterning defects) and 35% of these are also collapsed. The anterior microtubule organising center (MTOC) forms in stage 1 armi^72.1 oocytes. However, during stages 2-7 a posterior MTOC is not apparent in the mutant oocyte and microtubule levels in the oocyte and nurse cells are comparable, in contrast to wild-type egg chambers where the oocyte is enriched in microtubules compared to the nurse cells during these stages. Cortical microtubules persist at the posterior cortex of mid-oogenesis stage mutant oocytes, in contrast to wild type. (Cook et al., 2004) 45% of progeny derived from homozygous males mated to wild-type females hatch. 92% of eggs derived from armi^72.1 females lack dorsal appendages. (Tomari et al., 2004)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement Reference armi^72.1/armi¹ has lethal \| maternal effect \| embryonic stage phenotype, non-suppressible by lok^p6/lok^p6/lok^p6/lok^p6 (Orsi et al., 2010)
Phenotype Manifest In
Suppressed by
Statement Reference armi^72.1/armi¹ has dorsal appendage \| maternal effect phenotype, suppressible \| partially by mei-41^D3/mei-41^D3 (Klattenhoff et al., 2009) armi^72.1/armi¹ has dorsal appendage phenotype, suppressible \| partially by lok^p6/lok^p6/lok^p6/lok^p6 (Orsi et al., 2010) armi^72.1/armi¹ has dorsal appendage phenotype, suppressible \| partially by mei-41^D3/mei-41^D3 (Klattenhoff et al., 2007) armi^72.1/armi¹ has dorsal appendage phenotype, suppressible by lok^p6/lok^p6/lok^p6/lok^p6 (Klattenhoff et al., 2007) armi^72.1/armi¹ has microtubule organizing center & oocyte phenotype, suppressible by lok^p6/lok^p6/lok^p6/lok^p6 (Klattenhoff et al., 2007) armi^72.1/armi¹ has microtubule organizing center & oocyte phenotype, suppressible by mei-41^D3/mei-41^D3 (Klattenhoff et al., 2007)
NOT suppressed by
Statement Reference armi^72.1/armi¹ has dorsal appendage phenotype, non-suppressible by mei-W68¹/mei-W68^k05603 (Klattenhoff et al., 2007)
Additional Comments
Genetic Interactions
Statement Reference The dorsal appendage defects seen in eggs laid by armi[1]/armi[72.1] females are partly suppressed if the females are also homozygous for lok[p6]; 16.1% of the eggs have fused dorsal appendages, 7.3% lack dorsal appendages and 76.6% have wild-type dorsal appendages. (Orsi et al., 2010) 56% of eggs derived from mei-41[D3]/mei-41[D3] ; armi[1]/armi[72.1] double mutant females have normal dorsal appendages, but the fraction of embryos with normal dorsal appendages increases to 83% if the females are fed caffeine. (Klattenhoff et al., 2009) The fused dorsal appendage phenotype of armi^72.1/armi¹ eggs is suppressed in lok^p6; armi^72.1/armi¹ eggs with 92% of double mutants showing wild-type appendage morphology. The mei-41^D3 mutation partially suppresses the fused dorsal appendage phenotype of armi^72.1/armi¹ eggs; 56% of mei-41^D3; armi^72.1/armi¹ eggs show wild-type appendage morphology. The fused dorsal appendage phenotype of armi^72.1/armi¹ eggs is not suppressed in mei-W68¹/mei-W68^k05603; armi^72.1/armi¹ eggs. The microtubule-organizing center phenotype of armi^72.1/armi¹ oocytes is suppressed by the lok^p6 mutation. The microtubule-organizing center phenotype of armi^72.1/armi¹ oocytes is partially suppressed by the mei-41^D3 mutation. (Klattenhoff et al., 2007) armi^72.1 osk¹ double mutant ovaries have microtubule defects that are cytologically identical to the armi single mutant phenotype. (Cook et al., 2004)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	armi^72.1 is rescued by Scer\GAL4^elav-C155/armi^{Scer\UAS.P\T.T:Avic\GFP-EGFP} (Ashraf et al., 2006)
Partially rescued by	armi^72.1 is partially rescued by Scer\GAL4^nos.PG/armi^{Scer\UAS.P\T.T:Avic\GFP-EGFP} (Cook et al., 2004)
Comments
Stocks ( 1 )
Bloomington	8544 w^*; armi^72.1/TM6C, Sb¹ Tb¹
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	armi^72.1 (Klattenhoff et al., 2007, Ashraf et al., 2006, Vagin et al., 2006, Ashraf et al., 2006, Tadros et al., 2007, Klattenhoff et al., 2009, Orsi et al., 2010, Olivieri et al., 2010, Nagao et al., 2010, Rouget et al., 2010)
Name Synonym
Secondary FlyBase IDs

References ( 15 )
Research paper	Nagao et al., 2010, RNA 16(12): 2503--2515 Biogenesis pathways of piRNAs loaded onto AGO3 in the Drosophila testis. [FBrf0212366] Olivieri et al., 2010, EMBO J. 29(19): 3301--3317 An in vivo RNAi assay identifies major genetic and cellular requirements for primary piRNA biogenesis in Drosophila. [FBrf0212004] Orsi et al., 2010, J. Cell Sci. 123(20): 3515--3524 Drosophila I-R hybrid dysgenesis is associated with catastrophic meiosis and abnormal zygote formation. [FBrf0212012] Rouget et al., 2010, Nature 467(7319): 1128--1132 Maternal mRNA deadenylation and decay by the piRNA pathway in the early Drosophila embryo. [FBrf0212183] Klattenhoff et al., 2009, Cell 138(6): 1137--1149 The Drosophila HP1 homolog Rhino is required for transposon silencing and piRNA production by dual-strand clusters. [FBrf0208800] Klattenhoff et al., 2007, Dev. Cell 12(1): 45--55 Drosophila rasiRNA pathway mutations disrupt embryonic axis specification through activation of an ATR/Chk2 DNA damage response. [FBrf0192439] Tadros et al., 2007, Dev. Cell 12(1): 143--155 SMAUG is a major regulator of maternal mRNA destabilization in Drosophila and its translation is activated by the PAN GU kinase. [FBrf0192711] Ashraf et al., 2006, Cell 124(1): 191--205 Synaptic protein synthesis associated with memory is regulated by the RISC pathway in Drosophila. [FBrf0189896] Vagin et al., 2006, Science 313(5785): 320--324 A distinct small RNA pathway silences selfish genetic elements in the germline. [FBrf0194520] Forstemann et al., 2005, PLoS Biol. 3(7): e236 Normal microRNA maturation and germ-line stem cell maintenance requires Loquacious, a double-stranded RNA-binding domain protein. [FBrf0188210] Cook et al., 2004, Cell 116(6): 817--829 The Drosophila SDE3 homolog armitage is required for oskar mRNA silencing and embryonic axis specification. [FBrf0174441] Perrini et al., 2004, Mol. Cell 15(3): 467--476 HP1 controls telomere capping, telomere elongation, and telomere silencing by two different mechanisms in Drosophila. [FBrf0180524] Tomari et al., 2004, Cell 116(6): 831--841 RISC assembly defects in the Drosophila RNAi mutant armitage. [FBrf0174442]
Supplementary material	Ashraf et al., 2006, Cell 124(1): Supplemental Data. [FBrf0198682] Vagin et al., 2006, Science 313(5785): Supporting Online Material. [FBrf0198717]

Allele Dmel\armi72.1

Allele Dmel\armi^72.1