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Allele Dmel\beat-Ia³

General Information
Symbol	Dmel\beat-Ia3	Species	D. melanogaster
Name		FlyBase ID	FBal0057747
Feature type	allele	Associated gene	Dmel\beat-Ia
Also Known As	beat3
Allele class	loss of function allele
Mutagen	ethyl methanesulfonate
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 (Fambrough and Goodman, 1996)
Mutagen	ethyl methanesulfonate (Fambrough and Goodman, 1996, Ashburner et al., 1999.10.12)
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
Phenotype Manifest In
	A1-7 dorsal acute muscle 1 (with beat-IaC163) (Siebert et al., 2009) A1-7 dorsal acute muscle 2 (with beat-IaC163) (Siebert et al., 2009) A1-7 dorsal oblique muscle 1 (with beat-IaC163) (Siebert et al., 2009) A1-7 ventral longitudinal muscle 1 (with beat-IaC163) (Siebert et al., 2009) A1-7 ventral longitudinal muscle 2 (with beat-IaC163) (Siebert et al., 2009) A1-7 ventral longitudinal muscle 3 (with beat-IaC163) (Siebert et al., 2009) A1-7 ventral longitudinal muscle 4 (with beat-IaC163) (Siebert et al., 2009) A2-7 dorsal oblique muscle 2 (with beat-IaC163) (Siebert et al., 2009) abdominal intersegmental nerve (Kaufmann et al., 1998) abdominal segmental nerve (Fambrough and Goodman, 1996) Bolwig organ (Holmes and Heilig, 1999) motor neuron (Fambrough and Goodman, 1996) photoreceptor (Holmes and Heilig, 1999)
Detailed Description
	Statement Reference beat-Ia[3]/beat-Ia[C163] third instar larvae often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (31%), muscle 9 (34%), muscle 2 (8%), muscle 10 (13%). beat-Ia[3]/beat-Ia[C163] third instar larvae often lack neuromuscular junctions (NMJs) on ventral muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 12 (25%), muscle 13 (34%), muscle 6 (38%), muscle 7 (55%). (Siebert et al., 2009) Cells of the Bolwig's organs (BOs) form in homozygous embryos, but the morphology of the larval visual system (LVS) is severely disrupted and increased numbers of photoreceptor cells are apparent from the earliest stages of LVS development. Extra photoreceptor cells are seen both in the normal location of the BO clusters and dispersed between the two clusters. Embryos sometimes contain three BO's and, rarely, four BO clusters are seen. Migration of the BOs appears relatively normal in some embryos, but in others it is disrupted and the BO does not achieve its proper location even though head involution appears normal, or the BO is elongated. (Holmes and Heilig, 1999) Motor axons exit the CNS normally but then fail to branch and enter their muscle domains once in the periphery. The SNb fails to diverge from the ISN either completely (full bypass), 45% segments, or partially (partial bypass), 39% segments, the SNc fails to diverge in 77% segments. (Fambrough and Goodman, 1996)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Other
Statement Reference SoxNGA1192, beat-Ia[+]/beat-Ia3 has partially lethal - majority die phenotype (Girard et al., 2006)
Phenotype Manifest In
NOT Enhanced by
Statement Reference beat-IaC163/beat-Ia3 has A1-7 dorsal acute muscle 1 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A1-7 dorsal acute muscle 1 phenotype, non-enhanceable by Scer\GAL4Mef2.PR (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A1-7 dorsal acute muscle 2 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A1-7 dorsal acute muscle 2 phenotype, non-enhanceable by Scer\GAL4Mef2.PR (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A1-7 dorsal oblique muscle 1 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A1-7 dorsal oblique muscle 1 phenotype, non-enhanceable by Scer\GAL4Mef2.PR (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A2-7 dorsal oblique muscle 2 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B (Siebert et al., 2009) beat-IaC163/beat-Ia3 has A2-7 dorsal oblique muscle 2 phenotype, non-enhanceable by Scer\GAL4Mef2.PR (Siebert et al., 2009)
Other
Statement Reference SoxNGA1192, beat-Ia[+]/beat-Ia3 has anterior commissure phenotype (Girard et al., 2006) SoxNGA1192, beat-Ia[+]/beat-Ia3 has longitudinal connective phenotype (Girard et al., 2006) SoxNGA1192, beat-Ia[+]/beat-Ia3 has posterior commissure phenotype (Girard et al., 2006)
Additional Comments
Genetic Interactions
Statement Reference The neuromuscular junction innervation defects seen in the dorsal muscles of beat-Ia[3]/beat-Ia[C163] third instar larvae are not enhanced by expression of side[Scer\UAS.cSa] under the control of either Scer\GAL4[how-24B] or Scer\GAL4[Mef2.PR]. (Siebert et al., 2009) beat-Ia/+, SoxNGA1192/+ double heterozygous embryos commissures are partially fused and the longitudinal connectives are thinner or missing. This phenotype is not seen in either beat-Ia/+ or SoxNGA1192/+ embryos. (Girard et al., 2006) beat-Ia2/beat-Ia3 Rac1N17.Scer\UAS Scer\GAL4elav-C155 double mutant embryos exhibit additive, not synergistic effects on the ISNb full bypass phenotype. (Kaufmann et al., 1998) In beat-Ia2/beat-Ia3 transheterozygotes the SNb fails to diverge from the ISN completely (full bypass) in 38% segments or partially (partial bypass) in 28% segments. The SNb divergence defect can be suppressed by Fas2e76 and the SNc defect by ConFvex238. (Fambrough and Goodman, 1996)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	beat-Ia3 is rescued by Scer\GAL4elav-C155/beat-IaScer\UAS.cFa (Fambrough and Goodman, 1996) beat-IaC163/beat-Ia3 is rescued by beat-IaScer\UAS.cFa/Scer\GAL4elav.PLu (Siebert et al., 2009) beat-IaC163/beat-Ia3 is rescued by beat-IaScer\UAS.cFa/Scer\GAL4Fas2-Mz507 (Siebert et al., 2009)
Not rescued by	beat-IaC163/beat-Ia3 is not rescued by beat-IaScer\UAS.cFa/Scer\GAL4Mef2.PR (Siebert et al., 2009)
Comments	Scer\GAL4elav-C155 mediated expression of beat-IaScer\UAS.cFa rescues the SNb divergence defect. (Fambrough and Goodman, 1996)
Stocks ( 1 )
Bloomington	4748 w*; beat-Ia3 Fas3E25/CyO, P{act-lacZ.B}CB1
Notes on Origin
Discoverer
External Crossreferences & Linkouts
Other Crossreferences
Linkouts
Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	beat3 (Ashburner et al., 1999.10.12, Holmes and Heilig, 1999, Kaufmann et al., 1998, Fambrough and Goodman, 1996, Siebert et al., 2009) beat-Ia3 (Girard et al., 2006)
Name Synonym
Secondary FlyBase IDs
References ( 6 )
Research paper	Siebert et al., 2009, Genes Dev. 23(9): 1052--1062 Drosophila motor axons recognize and follow a Sidestep-labeled substrate pathway to reach their target fields. [FBrf0207941] Girard et al., 2006, Dev. Biol. 299(2): 530--542 Chromatin immunoprecipitation reveals a novel role for the Drosophila SoxNeuro transcription factor in axonal patterning. [FBrf0194303] Holmes and Heilig, 1999, Development 126(2): 261--272 Fasciclin II and beaten path modulate intercellular adhesion in Drosophila larval visual organ development. [FBrf0106663] Kaufmann et al., 1998, Development 125(3): 453--461 Drosophila Rac1 controls motor axon guidance. [FBrf0100716] Fambrough and Goodman, 1996, Cell 87(6): 1049--1058 The Drosophila beaten path gene encodes a novel secreted protein that regulates defasciculation at motor axon choice points. [FBrf0091058]
Personal communication to FlyBase	Ashburner et al., 1999.10.12, Adh. Adh. [FBrf0112153]