Allele Dmel\Liprin-α^F

General Information
Symbol	Dmel\Liprin-α^F	Species	D. melanogaster
Name		FlyBase ID	FBal0193542
Feature type	allele	Associated gene	Dmel\Liprin-α

Allele class
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	ethyl methanesulfonate (Choe et al., 2006)
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
Cytology
Phenotypic Data
Phenotypic Class
	lethal (with Liprin-α^E) (Prakash et al., 2009) neuroanatomy defective \| somatic clone (Choe et al., 2006)
Phenotype Manifest In
	eye photoreceptor cell \| somatic clone (Choe et al., 2006) optic cartridge \| somatic clone (Choe et al., 2006)
Detailed Description
	Statement Reference Liprin-α^F mutants exhibit a specific pattern of disruption in the structure of the cartridge, the synaptic unit in the lamina. Some cartridges have either >6 or <6 R cells axons, and some adjacent cartridges fuse. R-cells proliferate normally during the third instar larval stage in Liprin-α^F eye-specific mosaics and display normal morphological differentiation during pupal and adult stages. Liprin-α^F mutant R cell axons select appropriate ganglion-specific targets in the lamina and the medulla and induce appropriate neuronal differentiation in the lamina target field. These axons also elaborate topographically appropriate maps in each region, with glial cell differentiation in these areas also appearing largely normal. The behaviour of Liprin-α^F mutant axons (generated through MARCM) is indistinguishable from wild-type along their trajectories into the lamina plexus, with each axon remaining tightly associated with the axon bundle of its wild-type neighbours from the same ommatidium. However, once within the lamina plexus, unlike wild-type R cells, Liprin-α^F mutant R cells typically display specific defects in axon extension toward their targets. Two types of defect are observed. Approximately 64% of Liprin-α^F mutant axons completely fail to extend away from the ommatidial bundle, whereas 21% make weak, morphologically abnormal extensions; the remaining axons extend normally. All R cell subtypes are equally affected. (Choe et al., 2006)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Liprin-α^F/Liprin-α^E has lethal phenotype, suppressible \| partially by CadN[+]/CadN^Δ14 (Prakash et al., 2009) Liprin-α^F/Liprin-α^E has lethal phenotype, suppressible \| partially by Lar²¹²⁷/Lar[+] (Prakash et al., 2009)
Other
Statement Reference CadN[+]/CadN^Δ14, Lar²¹²⁷/Lar[+], Liprin-α^F has partially lethal - majority die \| dominant phenotype (Prakash et al., 2009)
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to rescue	Liprin-α^F fails to rescue Liprin-α¹ (Choe et al., 2006)
Comments	Liprin-α^F fails to complement the recessive lethal phenotype of Liprin-α¹. (Choe et al., 2006)
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	Liprin-α^F (Prakash et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 2 )
Research paper	Prakash et al., 2009, Dev. Biol. 336(1): 10--19 Complex interactions amongst N-cadherin, DLAR, and Liprin-alpha regulate Drosophila photoreceptor axon targeting. [FBrf0209258] Choe et al., 2006, Proc. Natl. Acad. Sci. U.S.A. 103(31): 11601--11606 Liprin-alpha is required for photoreceptor target selection in Drosophila. [FBrf0195369]

Allele Dmel\Liprin-αF

Allele Dmel\Liprin-α^F