A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\mbcD11.2

General Information
SymbolDmel\mbcD11.2SpeciesD. melanogaster
NameFlyBase IDFBal0063880
Feature typealleleAssociated geneDmel\mbc
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0063880 FBal0063877 FBal0063879 FBal0063878
Allele classloss of function allele
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
point mutation
comment=nucleotide position inferred by curator based on amino acid change reported in Figure 2 of FBrf0094649; mutations characterized in FBrf0094649 are reported to be GC to AT transitions at single nucleotides
evidence=experimental
reported_pr_change=E97@|FBrf0094649
na_change=G19617913T
pr_change=E96@|mbc-PA
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Amino acid replacement: W97@.
Nucleotide substitution: G?A.
TGG to TAG nucleotide change.
Amino acid replacement: E97@.
Cytology
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Statement
Reference
In homozygous mutant embryos, myoblasts are competent to migrate to the founder cells, but fusion does not occur. Homozygous embryos exhibit breaks in the outer longitudinal fascicles and a collapse of axons onto the MP1 fascicle tracts. Thinning of the longitudinal axon tracts and abnormal spacing between segments is also observed.
Unfused myoblasts are apparent in stage 16 homozygous embryos. Although the majority of founder cells examined remain mononucleate, a limited amount of fusion does occur, as binucleate muscle precursors that have undergone a single fusion event between a founder cell and a fusion competent myoblast (FCM) are seen in the mutant embryos. The muscle founders analysed and the percentage of segments in which the founder cell remains mononucleate are as follows: DA1 (72.1%), DO1 (76.3%), LO1 (90.2%), LT2 (93.4%), LT4 (95.0%), VT1 (78.9%), VA2 (84.6%). The overall level of myoblast fusion in embryos lacking both maternal and zygotic function is roughly comparable to that seen in zygotic mutant embryos. The F-actin foci which are seen in wild-type FCMs at points of contact with developing myofibers are less dense and somewhat dispersed in homozygous FCMs. In addition, the actin cytoskeletal network of the mutant FCMs is different from wild type, with many of the mutant cells showing a complete collapse of the network.
The eve-expressing DA1 founder cell undergoes no fusion in mbc[D11.2] embryos.
Myoblast fusion is absent in mbc[D11.2] zygotic mutant embryos and in embryos derived from mbc[D11.2] germline clones.
The extent of myoblast fusion in mbcD11.2 mutant embryos is significantly reduced compared to wild type.
Homozygous embryos do not show any apparent defects in macrophage migration.
When mutant somatic clones are made in border cells, a strong effect is seen on border cell migration. At stage 10 only about 10% of mutant border cell clusters reach the oocyte.
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Statement
Reference
mbcD11.2 has embryonic myoblast phenotype, non-enhanceable by spg2
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Reference
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Reference
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Statement
Reference
mbcD11.2 is a suppressor of centripetally migrating follicle cell & actin filament phenotype of Pvrλ.Scer\UAS.T:Hsap\MYC, Scer\GAL4slbo.2.6
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Statement
Reference
In mbc[D11.2]/mbc[D11.2], spg[2]/spg[2] double mutants, myoblasts fail to fuse but still cluster around the founder cells (as in mbc[D11.2]/mbc[D11.2] mutants). There is no significant increase in broken fascicles or the collapse of the outer longitudinal tracts in mbc[D11.2], spg[2] double mutants over mbc[D11.2] mutants alone. However, there is an increase in midline fascicle crossing in the double mutants. Abnormal positioning of the ventral nerve cord is also observed in the double mutants. mbc[D11.2], Df(2L)CadN[Δ14] embryos do not show increased axonal outgrowth or guidance defects compared to mbc[D11.2] embryos.
Expression of Rac1[V12.Scer\UAS] under the control of Scer\GAL4[sns.PK] rescues myoblast fusion in homozygous mbc[D11.2] embryos such that the somatic muscle pattern is almost wild type. Expression of Rac1[V12.Scer\UAS] under the control of Scer\GAL4[kirre-rP298] does not rescue myoblast fusion in homozygous mbc[D11.2] embryos. Expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[sns.PK] does not rescue myoblast fusion in homozygous mbc[D11.2] embryos. mbc[D11.2] spg[2] double mutant embryos have a roughly comparable overall level of myoblast fusion compared to mbc[D11.2] single mutant embryos.
The rough eye phenotype resulting from Scer\GAL4[GMR.PU]-mediated expression of Ced-12[Scer\UAS.cGa] and mbc[Scer\UAS.cBa] is suppressed by heterozygosity for mbc[D11.2].
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Rescued by
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Comments
Expression of either mbc[Scer\UAS.T:Ivir\HA1] or mbc[NPxxP.Δ1807.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[sns.PK] restores fusion in mbc[D11.2] embryos and a wild-type somatic muscle pattern is formed. Myoblast fusion remains severely impaired in mbc[D11.2] embryos expressing mbc[Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[kirre-rP298]. These embryos show a roughly twofold increase in muscle precursor formation (where a single fusion event between a founder cell and a fusion competent myoblast has occurred) compared to mbc[D11.2] embryos.
Expression of mbc[Scer\UAS.T:Ivir\HA1] rescues the myoblast fusion defect in mbc[D11.2] embryos when expressed using Scer\GAL4[twi.PG] or Scer\GAL4[how-24B] but not Scer\GAL4[kirre-rP298]. Scer\GAL4[twi.PG]-mediated expression of mbc[SH3W47K.Scer\UAS.T:Ivir\HA1] fails to rescue the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]-mediated expression of mbc[DockerF6.4.Scer\UAS.T:Ivir\HA1] fails to rescue the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]- or Scer\GAL4[how-24B]-mediated expression of mbc[CBS.Scer\UAS] rescues the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]- or Scer\GAL4[how-24B]-mediated expression of mbc[Δ1807.Scer\UAS.T:Ivir\HA1] rescues the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]- or Scer\GAL4[how-24B]-mediated expression of mbc[NPxxP.Scer\UAS.T:Ivir\HA1] rescues the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]- or Scer\GAL4[how-24B]-mediated expression of mbc[NPxxP.Δ1807.Scer\UAS.T:Ivir\HA1] rescues the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]- or Scer\GAL4[how-24B]-mediated expression of mbc[ΔPRM.Scer\UAS.T:Ivir\HA1] rescues the mbc[D11.2] myoblast fusion defect. Scer\GAL4[twi.PG]- or Scer\GAL4[how-24B]-mediated expression of mbc[ΔDHR1.Scer\UAS.T:Ivir\HA1] fails to rescue the mbc[D11.2] myoblast fusion defect.
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Bloomington
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Reported As
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hide References ( 18 )
Research paper
Biersmith et al., 2011, PLoS ONE 6(1): e16120
The DOCK Protein Sponge Binds to ELMO and Functions in Drosophila Embryonic CNS Development. [FBrf0212890]
Haralalka et al., 2011, Development 138(8): 1551--1562
Asymmetric Mbc, active Rac1 and F-actin foci in the fusion-competent myoblasts during myoblast fusion in Drosophila. [FBrf0213340]
Bulchand et al., 2010, PLoS ONE 5(2): e9374
The intracellular domain of dumbfounded affects myoblast fusion efficiency and interacts with rolling pebbles and loner. [FBrf0210103]
Shelton et al., 2009, Development 136(7): 1159--1168
The immunoglobulin superfamily member Hbs functions redundantly with Sns in interactions between founder and fusion-competent myoblasts. [FBrf0207479]
Geisbrecht et al., 2008, Dev. Biol. 314(1): 137--149
Drosophila ELMO/CED-12 interacts with Myoblast city to direct myoblast fusion and ommatidial organization. [FBrf0202723]
Massarwa et al., 2007, Dev. Cell 12(4): 557--569
WIP/WASp-based actin-polymerization machinery is essential for myoblast fusion in Drosophila. [FBrf0201865]
Balagopalan et al., 2006, Mol. Cell. Biol. 26(24): 9442--9455
The CDM superfamily protein MBC directs myoblast fusion through a mechanism that requires phosphatidylinositol 3,4,5-triphosphate binding but is independent of direct interaction with DCrk. [FBrf0194774]
Menon et al., 2005, J. Cell Biol. 169(6): 909--920
A positive feedback loop between dumbfounded and rolling pebbles leads to myotube enlargement in Drosophila. [FBrf0187819]
Wilson et al., 2005, Development 132(3): 491--501
FGF signalling and the mechanism of mesoderm spreading in Drosophila embryos. [FBrf0183935]
Galletta et al., 2004, Mech. Dev. 121(12): 1455--1468
SNS: adhesive properties, localization requirements and ectodomain dependence in S2 cells and embryonic myoblasts. [FBrf0180484]
Gallio et al., 2004, Development 131(15): 3605--3614
Rhomboid 3 orchestrates Slit-independent repulsion of tracheal branches at the CNS midline. [FBrf0179216]
Ishimaru et al., 2004, EMBO J. 23(20): 3984--3994
PVR plays a critical role via JNK activation in thorax closure during Drosophila metamorphosis. [FBrf0180198]
Paladi and Tepass, 2004, J. Cell Sci. 117(26): 6313--6326
Function of Rho GTPases in embryonic blood cell migration in Drosophila. [FBrf0187835]
Duchek et al., 2001, Cell 107(1): 17--26
Guidance of cell migration by the Drosophila PDGF/VEGF receptor. [FBrf0139607]
Menon and Chia, 2001, Dev. Cell 1(5): 691--703
Drosophila rolling pebbles: a multidomain protein required for myoblast fusion that recruits D-Titin in response to the myoblast attractant Dumbfounded. [FBrf0141462]
Bour et al., 2000, Genes Dev. 14(12): 1498--1511
Drosophila SNS, a member of the immunoglobulin superfamily that is essential for myoblast fusion. [FBrf0128410]
Erickson et al., 1997, J. Cell Biol. 138(3): 589--603
Drosophila myoblast city encodes a conserved protein that is essential for myoblast fusion, dorsal closure, and cytoskeletal organization. [FBrf0094649]
Supplementary material
Ishimaru et al., 2004, EMBO J. 23(20):
Supplementary data. [FBrf0182966]