Allele Dmel\Abi^P2

General Information
Symbol	Dmel\Abi^P2	Species	D. melanogaster
Name		FlyBase ID	FBal0239155
Feature type	allele	Associated gene	Dmel\Abi

Allele class	loss of function allele
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	loss of function allele (Lin et al., 2009)
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
Caused by insertion	P{EP}Abi^P2 (Lin et al., 2009)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| pupal stage (with Abi^KO) (Lin et al., 2009) lethal \| pupal stage (with Df(3R)JY19) (Lin et al., 2009) neuroanatomy defective \| embryonic stage (with Abi^KO) (Lin et al., 2009) neuroanatomy defective \| embryonic stage \| maternal effect, with Df(3R)JY19/Abi^P1 (Lin et al., 2009)
Phenotype Manifest In
	longitudinal connective (with Abi^KO) (Lin et al., 2009) longitudinal connective \| maternal effect, with Df(3R)JY19/Abi^P1 (Lin et al., 2009)
Detailed Description
	Statement Reference Embryos maternally hypomorphic for Abi function and lacking zygotic Abi function (derived from Abi[P1]/Df(3R)JY19 females mated to Abi[P2] carrying males) have deranged longitudinal connectives and commissural tracts. 57.1% of these embryos have midline crossing defects in ipsilateral axon fascicles at stage 17. 9.6% of Abi[KO]/Abi[P2] embryos have midline crossing defects in ipsilateral axon fascicles at stage 17. (Lin et al., 2009)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Abi^P2/Abi^KO has neuroanatomy defective \| embryonic stage phenotype, suppressible \| partially by Abl⁴/Abl[+] (Lin et al., 2009)
Suppressor of
Statement Reference Abi[+]/Abi^P2 is a suppressor \| partially of neuroanatomy defective \| embryonic stage phenotype of Abl⁴/Abl¹ (Lin et al., 2009)
Phenotype Manifest In
Suppressed by
Statement Reference Abi^P2/Abi^KO has longitudinal connective phenotype, suppressible \| partially by Abl⁴/Abl[+] (Lin et al., 2009)
Suppressor of
Statement Reference Abi[+]/Abi^P2 is a suppressor \| partially of longitudinal connective phenotype of Abl⁴/Abl¹ (Lin et al., 2009)
Additional Comments
Genetic Interactions
Statement Reference The frequency of the midline crossing defect seen in Fas-expressing axons in Abl[1]/Abl[4] embryos is suppressed from 37% to 18% by Abi[P2]/+. The frequency of the midline crossing defect seen in Fas-expressing axons in Abi[KO]/Abi[P2] embryos is suppressed from 9.6% to 3% by Abl[4]/+. (Lin et al., 2009)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Precise excision of the insertion reverts the lethal phenotype. (Lin et al., 2009)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	Abi^P2 abi^P2 (Lin et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 1 )
Research paper	Lin et al., 2009, Development 136(18): 3099--3107 Abi plays an opposing role to Abl in Drosophila axonogenesis and synaptogenesis. [FBrf0208583]

Allele Dmel\AbiP2

Allele Dmel\Abi^P2