Aberration Dmel\Df(4)C3

General Information
Symbol	Dmel\Df(4)C3	Species	D. melanogaster
Name		FlyBase ID	FBab0028454
Feature type	chromosomal_deletion

Computed Breakpoints include	102D6;102F
Deleted segment	102D6--102F
Sequence coordinates
Recent Updates
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FB2012_01
FB2011_10
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to progenitor)	chromosomal_deletion (Winberg et al., 1998)
Breakpoints	102D6;102F (Winberg et al., 1998)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data	bk1 << plexA << bk2
Genetic mapping information
Comments
Comments on Cytology
	All limits from polytene analysis (FBrf0105958)
Sequence Crossreferences
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name
Gene Deletion & Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted	plexA (Winberg et al., 1998, Yu et al., 2010)
Molecular Data
Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
Genes Duplicated
Complementation Data
Molecular Data
Genes NOT Duplicated
Complementation Data
Molecular Data
Related Comments

Phenotypic Data
In combination with other aberrations	41.9% of hemisegments in Df(4)C3/+ ; Df(3R)swp2^MICAL/+ double heterozygotes show defects in muscle 6/7 innervation and 33.0% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 44.6% of hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. (Terman et al., 2002)
NOT in combination with other aberrations	Most homozygous Df(4)C3 mutants die at late embryonic stage, although some mutants reach the third-instar larval stage. R1-R6 growth cones scatter around the lamina termination region in Df(4)C3 homozygous third instar larvae, leading to the appearance of a discontinuous termination layer in the lamina. (Yu et al., 2010) Df(4)C3 homozygous embryos exhibit defects in the innervation of the ventral muscles in most of the segments examined. The most distal SNa axon is often unable to separate from the dorsal SNa bundle in Df(4)C3 homozygous embryos and so fails to innervate muscle 24, resulting in a 'stall' phenotype. In Df(4)C3 mutants, the outermost fascicle visible with Fas2 is reduced in thickness and is discontinuous along its entire length. (Ayoob et al., 2006) 60.8% of homozygous hemisegments show defects in muscle 6/7 innervation and 47.3% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 74.3% of homozygous hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. (Terman et al., 2002) Mutants exhibit an axon guidance phenotype. The SNa often branches abnormally, and the ISNb nerve also sometimes branches abnormally. (Winberg et al., 2001) Homozygous embryos show axon guidance defects both in the central nervous system and in the projections of motor nerves to their muscle targets in the periphery. ISNb growth cones often fail to defasciculate from one another at any or all three of the ISNb choice points. Occasionally they fail to exit the intersegmental nerve (ISN) and therefore bypass the ventral muscles, in some cases they innervate their ventral muscle targets via small projections made directly from the main branch of the ISN. More often, they exit the ISN but fail to defasciculate at choice points 2 and/or 3, leading to a thickened, stalled nerve branch and failure to innervate muscles 6 and 7 and/or 12. The segmental nerve is also often abnormal; SNa axons fail to defasciculate from one another at the second choice point in approximately 70% of segments and instead extend dorsally as a single branch. The outermost Fas2-positive longitudinal connective is often disrupted and is sometimes fused with the middle Fas2-positive longitudinal connective. Growth cones from the transverse nerve extend ectopic projections onto ventral muscles in 36.5% of segments. (Winberg et al., 1998)
Stocks ( 1 )
Bloomington	7083 w^*; Df(4)C3/In(4)ci^D, ci^D pan^ciD sv^spa-pol
Notes on Origin
Discoverer	S. Flister W. Gehring (Winberg et al., 1998)

Balancer / Genotype Variants of the Aberration

Separable Components

Other Comments

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	Df(4)C3 (Ayoob et al., 2004, Yu et al., 2010) Df(4)C3^PlexA (Terman et al., 2002) plexA^Df(4)C3 (Ayoob et al., 2006) PlexA^Df(4)C3 (Yu et al., 2010)
Name Synonym
Secondary FlyBase IDs

References ( 10 )
Research paper	Yu et al., 2010, J. Neurosci. 30(36): 12151--12156 Plexin a-semaphorin-1a reverse signaling regulates photoreceptor axon guidance in Drosophila. [FBrf0211784] Ayoob et al., 2006, Development 133(11): 2125--2135 Drosophila Plexin B is a Sema-2a receptor required for axon guidance. [FBrf0190270] Ayoob et al., 2004, J. Neurosci. 24(30): 6639--6649 The Drosophila receptor guanylyl cyclase Gyc76C is required for semaphorin-1a-plexin A-mediated axonal repulsion. [FBrf0179119] Terman et al., 2002, Cell 109(7): 887--900 MICALs, a family of conserved flavoprotein oxidoreductases, function in plexin-mediated axonal repulsion. [FBrf0151231] Winberg et al., 2001, Neuron 32(1): 53--62 The transmembrane protein off-track associates with plexins and functions downstream of semaphorin signaling during axon guidance. [FBrf0139778] Winberg et al., 1998, Cell 95(7): 903--916 Plexin A is a neuronal semaphorin receptor that controls axon guidance. [FBrf0105958]
Abstract	Locke et al., 2004, A. Dros. Res. Conf. 45: 891C Matching mutations to genes on chromosome 4 of Drosophila. [FBrf0174175] Locke et al., 2003, A. Dros. Res. Conf. 44: 990C Molecular Mapping of Deletions on Chromosome 4 of Drosophila. [FBrf0154970] Vining et al., 2002, A. Dros. Res. Conf. 43: 689B D-Sema2a is required to position the Drosophila embryonic salivary gland. [FBrf0146209]
FlyBase analysis	FlyBase, 2007, En masse symbol-based assigment of Aberration Class with respect to wild type. En masse symbol-based assigment of Aberration Class with respect to wild type. [FBrf0191808]