Allele Dmel\armi¹

General Information
Symbol	Dmel\armi¹	Species	D. melanogaster
Name		FlyBase ID	FBal0155637
Feature type	allele	Associated gene	Dmel\armi

Allele class
Mutagen
Recent Updates
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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
Mutagen
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 Insertion in the 5' UTR of armi. (Cook et al., 2004)
Caused by insertion	P{lacW}armi¹ (Cook et al., 2004)
Cytology
Phenotypic Data
Phenotypic Class
	female sterile (Cook et al., 2004) lethal \| embryonic stage \| maternal effect (with armi^72.1) (Orsi et al., 2010) male sterile \| partially (Tomari et al., 2004)
Phenotype Manifest In
	dorsal appendage (with armi^72.1) (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 armi^72.1) (Klattenhoff et al., 2009) microtubule organizing center & oocyte (with armi^72.1) (Klattenhoff et al., 2007)
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) Homozygous females produce eggs where 67% completely lack dorsal appendages (indicating strong dorsal/ventral patterning defects). (Cook et al., 2004) 75% of progeny derived from homozygous males mated to wild-type females hatch. 67% of eggs derived from armi¹ females lack dorsal appendages, while some of the eggs have wild-type or partially fused 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) armi¹ 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
Partially rescued by	armi¹ 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	8513 y¹ w^*; P{lacW}armi¹/TM3, Sb¹
Notes on Origin
Discoverer

Comments
	Excision of the insertion can revert the mutant phenotype. (Cook et al., 2004)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	armi¹ (Klattenhoff et al., 2007, 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 ( 12 )
Research paper	Klenov et al., 2011, Proc. Natl. Acad. Sci. U.S.A. 108(46): 18760--18765 Separation of stem cell maintenance and transposon silencing functions of Piwi protein. [FBrf0216776] 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] 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]

Allele Dmel\armi1

Allele Dmel\armi¹