Allele Dmel\mbcD11.2
| General Information | |||
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| Symbol | Dmel\mbcD11.2 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0063880 | |
| Feature type | allele | Associated gene | Dmel\mbc |
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| Allele class | loss of function allele | ||
| Mutagen | ethyl methanesulfonate | ||
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| Description |
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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
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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 | |||
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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 | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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Detailed Description
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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. | |||
External Data
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Interactions
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Phenotypic Class
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Enhanced by | |||
Statement Reference | |||
NOT Enhanced by | |||
Statement Reference | |||
Phenotype Manifest In
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NOT Enhanced by | |||
Statement Reference | |||
Suppressed by | |||
Statement Reference | |||
NOT suppressed by | |||
Statement Reference mbcD11.2 has embryonic myoblast phenotype, non-suppressible by Scer\GAL4kirre-rP298/Rac1V12.Scer\UAS | |||
Enhancer of | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference mbcD11.2/mbc[+] is a suppressor of eye phenotype of Ced-12Scer\UAS.cGa, Scer\GAL4Mef2.PR, mbcScer\UAS.cBa mbcD11.2 is a suppressor of centripetally migrating follicle cell & actin filament phenotype of Pvrλ.Scer\UAS.T:Hsap\MYC, Scer\GAL4slbo.2.6 mbcD11.2 is a suppressor of centripetally migrating follicle cell phenotype of Pvrλ.Scer\UAS.T:Hsap\MYC, Scer\GAL4slbo.2.6 | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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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]. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Rescued by | |||
| Not rescued by | mbcD11.2/Df(3R)mbc9 is not rescued by Scer\GAL4how-24B/mbcΔDHR1.Scer\UAS.T:Ivir\HA1/Scer\GAL4how-24B | ||
| 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. | ||
Stocks
( 1 ) | |||
| Bloomington | |||
Notes on Origin
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| Discoverer | |||
External Crossreferences & Linkouts
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Synonyms & Secondary IDs
( 5 ) | |||
| Reported As | |||
| Symbol Synonym | D11.2 MbcD11.2 mbcD11.2 mbcDll.2 mbcD11.2 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 18 ) | |||
| Research paper |
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| Supplementary material |
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External Crossreferences & Linkouts