|Feature type||allele||Associated gene||Dmel\beat-Ia|
|Also Known As||beat3|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
beat-Ia/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/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%).
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.
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.
|Phenotype Manifest In|
|NOT Enhanced by|
beat-IaC163/beat-Ia3 has A1-7 dorsal acute muscle 1 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B
beat-IaC163/beat-Ia3 has A1-7 dorsal acute muscle 2 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B
beat-IaC163/beat-Ia3 has A1-7 dorsal oblique muscle 1 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B
beat-IaC163/beat-Ia3 has A1-7 dorsal oblique muscle 1 phenotype, non-enhanceable by Scer\GAL4Mef2.PR
beat-IaC163/beat-Ia3 has A2-7 dorsal oblique muscle 2 phenotype, non-enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B
The neuromuscular junction innervation defects seen in the dorsal muscles of beat-Ia/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].
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.
beat-Ia2/beat-Ia3 Rac1N17.Scer\UAS Scer\GAL4elav-C155 double mutant embryos exhibit additive, not synergistic effects on the ISNb full bypass phenotype.
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 6 )|
|Personal communication to FlyBase|