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General Information
Symbol
Dmel\Mhc10
Species
D. melanogaster
Name
FlyBase ID
FBal0012251
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Nucleotide change:

    G16783832A

    Reported nucleotide change:

    G?A

    Comment:

    Mutation in 3' splice acceptor from AG to AA

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    A single base pair change mutates the consensus 3' splice site of exon 15a from CAG to CAA.

    Expression Data
    Reporter Expression
    Additional Information
    Statement
    Reference
     
    Marker for
    Reflects expression of
    Reporter construct used in assay
    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 1 )
    Modifiers Based on Experimental Evidence ( 0 )
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Disease-implicated variant(s)
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In

    indirect flight muscle & myofibril

    indirect flight muscle & sarcomere

    indirect flight muscle & striated muscle thick filament

    indirect flight muscle & Z disc

    Detailed Description
    Statement
    Reference

    Mhc10 homozygotes bearing two copies of MhcS531P exhibit a progressive decline in flight ability. Indirect flight muscle (IFM) fibers show reduced power output (with lower work production and slow kinetics); actively beating IFMs exhibit decreased lattice spacing and decreased active number of cross-bridges.

    Mhc10 homozygotes bearing one copy of MhcS531P exhibit increased diastolic diameter in aged adults (3 weeks-old) but not in young adults (4 days-old).

    Indirect flight muscles of MhcDA2B/MhcDA2B, Mhc10/Mhc10 organisms fail to assemble properly and worsen with age: In late-stage pupae, there are poorly formed myofibrils with abnormal filament packing, and M- and Z-lines are extremely distorted. In 2h-old adults, there are severe defects in packing and alignment of filaments, with remnants of M- and Z-lines diffused throughout the sarcomere. In 2-days old adults, thick and thin filaments are dispersed randomly throughout the myofibril.

    Indirect flight muscles of MhcDA2B/+, Mhc10/+ organisms show abnormal myofibril morphology: In late-stage pupae there are small myofibrils that show some filament packing disruptions, and poorly-formed M- and Z-lines. In 2h-old adults, myofibrils show further disruption in thick and thin filament packing and M- and Z-lines are aberrant or absent. In 2d-old adults some myofibrils appear fused, with poorly ordered thick and thin filament arrays, and Z-lines are more closely spaced.

    Indirect flight muscles of MhcDA1/MhcDA1, Mhc10/Mhc10 organisms fail to assemble properly and worsen with age: In late-stage pupae, myofibrils are distorted with some disruptions of thick and thin filament packing, M- lines are poorly formed and Z-lines are diffuse. In 2h-old adults, more severe filament irregularities are present, with gaps between thick and thin filaments, aberrant filament alignment. In 2d old adults, adjacent myofibrils tend to merge.

    Indirect flight muscles of 2h and 2d old MhcDA1/+, Mhc10/+ show essentially normal myofibrils with occasional filaments missing from myofibrils that display similar to control M- and Z-lines. These muscles show decreased power output, slower kinetics and enhanced stiffness compared to controls.

    The overall morphology of DLM fibers in MhcR249Q/MhcR249Q, Mhc10/Mhc10 and MhcR249Q/+, Mhc10/Mhc10 adults is comparable to controls. At the ultrastructure level, MhcR249Q/MhcR249Q, Mhc10/Mhc10 individuals show no defects in late pupae and in 2h-old adults, but 2 days-old adults show minor degradation of the hexagonal packing around the fibre edges and 7 days-old adults show severe fiber disruption; MhcR249Q/+, Mhc10/Mhc10 individuals show no obvious defects.

    In both MhcR249Q/MhcR249Q, Mhc10/Mhc10 and MhcR249Q/+, Mhc10/Mhc10 adults, these indirect flight muscles have altered kinetics, including significant decreases in active tension, power generation and net work, but unaltered passive tension, as compared to controls. MhcR249Q/MhcR249Q, Mhc10/Mhc10 adults, but not MhcR249Q/+, Mhc10/Mhc10 adults show significantly altered cross-bridge kinetics, including decreased maximum frequency of muscle length oscillation, increased 2πc and decreased 2πb.

    MhcR249Q/+, Mhc10/Mhc10 individuals do nor show any obvious defects in DLM fibers.

    Both Mhc+t24.1 hetero- and homo-zygosity in a Mhc10 background is viable and adults can fly. In the Mhc+t24.1, Mhc10 double homozygosity condition, pupal and adult indirect flight muscles show regularly packed myofibrils, with six thin filaments around each thick filament and well-formed sarcomeres.

    MhcT178I or MhcY583S homozygosity in a Mhc10 background induces flightless phenotypes and adults typically display a wings-up phenotype; the heterozygosity conditions also lead to significant and progressive decreases in flight ability.

    In the MhcY583S, Mhc10 double homozygosity condition, pupal and 2h-old adult indirect flight muscles show regularly packed myofibrils, with six thin filaments around each thick filament and well-formed sarcomeres; however, 2 days-old adult indirect flight muscles show some disruption in myofibril morphology (thick and thin filaments disperse into neighboring myofibrils), and 7 days-old adult indirect flight muscles show continued filament dispersion (some fusion of neighboring myofibrils). In the MhcY583S/+, Mhc10/Mhc10 condition, the pupal and 2h-old adult indirect flight muscles show no obvious defects; however, 2 days-old adult indirect flight muscles show some disruption in myofibril morphology (thick and thin filaments beginning to disperse from myofibrils and possibly fusing with neighboring myofibrils); 7 days-old adult indirect flight muscles show thick and thin filaments merging into neighboring myofibrils.

    In the MhcT178I, Mhc10 double homozygosity condition, pupal indirect flight muscles show assembly defects with disrupted myofibril morphology (myofilament subdomains with myofibrils that are poorly aligned with each other and fraying of filaments); 2h-old adult indirect flight muscles show extreme disruption in morphology (thick filaments dispersed in myofibril remnants and reduction in regular sarcomere patterns); 2 days-old adult indirect flight muscles show continued disruption in myofibril morphology (no regular sarcomeric structures and Z-band material scattered throughout the myofibril remnants). In the MhcT178I/+, Mhc10/Mhc10 condition, the pupal and 2h-old adult indirect flight muscles show no obvious defects; however, 2 days-old adult indirect flight muscles show some disruption in myofibril morphology (myofilaments are missing from the lattice and the sarcomere structural elements are disrupted); in 7 days-old adults there is a severe muscle degeneration.

    Both MhcR672C hetero- and homo-zygosity in a Mhc10 background leads to a fully flightless phenotype; the MhcR672C homozygosity condition also typically leads to a wings-up phenotype.

    In the MhcR672C, Mhc10 double homozygosity condition, pupal indirect flight muscles display severe assembly defects (abnormally shaped and sized myofibrils, and aberrantly localized Z-band material, with poor myofilament organization); 2h-old adult indirect flight muscles show extreme disruption in morphology (thick filaments dispersed in myofibril remnants and reduction in regular sarcomere patterns); these defects become more severe during adulthood. In the MhcR672C/+, Mhc10/Mhc10 condition, pupal indirect flight muscles show no obvious defects; however, 2h-old adult indirect flight muscles present myofibrils with disrupted myofilament arrays and branching sarcomeres with wavy Z- and M-line material; 2 days-old adult indirect flight muscles show disrupted myofibril morphology with scattered Z-band material, and sarcomeres are further disordered; in 7 days-old adults there is a severe muscle degeneration.

    MhcK1728del/Mhc10 transheterozygous adults show significantly decreased jump and climbing abilities, display wing posture defects and fail to beat their wings, indicating a complete lack of flight ability; these are associated with severe sarcomere organization defects and atrophy of the indirect flight muscles.

    Indirect flight muscles in Mhc10/Mhc10, MhcR146N/MhcR146N females show normal sarcomere organization at late pupal stage and in 2h-old adults, minor disruptions of thick and thin filament packing in 2-days old adults, and disorder in myofibril morphology in 7-days old adults, including gaps in the hexagonal packing of thick and thin filaments and disruption in the Z- and M-lines, as compared to controls. These muscles also show significantly decreased power generation and work, significantly increased active tension, but do not show a significant change in passive tension, as compared to controls; under optimal power producing conditions, there are further significant decreases in power generation and net work, which is likely due to decreased work generated:work absorbed ratio, as well as in relative muscle length amplitude, as compared to controls. These muscle defects are associated with a progressive decrease in flight index and a lower wing beat frequency, as compared to controls. Mhc10/Mhc10, MhcR146N/+ individuals display similar, albeit more modest, flight ability defects and indirect flight muscle morphology and performance defects.

    The hearts of Mhc10/Mhc10, MhcR146N/+ individuals display significant decreases in cardiac dimensions (diastolic and systolic diameters) and in fractional shortening, and a significant increase in systolic interval, but do change in heart period, as compared to controls; the heart has an essentially normal myofibrillar integrity and organization in 1-week old adults, but displays myofibrillar discontinuities in 3-weeks old adults, as compared to controls; cardiomyocyte thickness in both young and aged mutant adults shows no statistically significant differences, as compared to controls.

    Adults bearing two copies of either MhcR1845W, MhcE1883K or MhcE1883K in an Mhc10 homozygous background present a wings-up phenotype, are virtually flightless, jump significantly shorter distances, and the indirect flight muscles exhibit severe disruptions in muscle fibers, including torn fibers that are bunched at the attachment sites, disrupted sarcomere integrity and accumulation of myosin and poly-ubiquitin aggregates, as compared to controls. At the ultrastructural level, the indirect flight muscles of pupae and young adults lack the normal round morphology, lack the regular sarcomeric arrangement and show misaligned subsections of myofibrils, with several areas showing disruption of the hexagonal arrangement of thick and thin filaments, as compared to controls; these defects are more severe in young adults compared to pupae.

    Flies expressing MhcP838L/MhcP838L in a Mhc10/Mhc10 background, exhibit impaired flight ability. The indirect flight muscles in 2 day old flies display largely normal myofibril morphology and sarcomeric structure, but a few show occasional minor abnormalities in Z-disk regularity. At 3 weeks post-eclosion, indirect flight muscles show areas with Z-band irregularities, sarcomere gaps, abnormalities in myofibrillar shape and orientation, and defects in myofilament packing, as compared with controls. 2-3 day old flies expressing MhcP838L/MhcP838L in a Mhc10/Mhc10 background show no significant difference in indirect flight muscle power, wing beat frequency, active stiffness, isometric tension or rigor stiffness as compared with controls (Mhc+t12.4/Mhc+t12.4 in a Mhc10/Mhc10 background).

    Female flies expressing MhcE701K in a homozygous Mhc10 background completely lack flight ability. Two day old flies are unable to beat their wings, and a "wings-up" phenotype is present. The jump ability of two day old females is also severely reduced compared with controls.

    Myosin isolated from the indirect flight muscles of flies expressing MhcE701K in a homozygous Mhc10 background has significantly reduced catalytic activity compared to control myosin. CaATPase, MgATPase, and actin-stimulated MgATPase activity (V[[max]]) and catalytic efficiency (the ratio of V[[max]] / actin affinity relative to ATPase (K[[m]]) ) are all reduced. K[[m]] is increased. The actin sliding velocity stimulated by mutant myosin is significantly reduced compared to that of control myosin.

    Myosin isolated from the indirect flight muscles of flies expressing MhcE701K in a Mhc10 mutant background has an increased propensity to aggregate compared to control myosin. The mutant myosin molecules have collapsed heads that frequently pack into aggregated clumps reminiscent of wild-type motors exposed to elevated temperatures. Only 22.5% of myosin exhibit the normal two headed structure.

    The indirect flight muscles of female flies expressing MhcE701K in a Mhc10 mutant background exhibit ultrastructural defects that become progressively worse with age. During the late pupal stages M-lines and Z-discs are distinguishable, but the myofibrils show disruption of integrity and lack the round shape seen in controls. In two hour old flies the myofibrils show loss of visible M-lines, with decreases in myofibril integrity and hexagonal packing. By two days old the myofibrils show severe ultrastructural deterioration, with broken and streaming Z-discs and a loss of thick filaments and M-lines. The fibers show sarcolemmal membrane invaginations and protrusions and contain rimmed vacuoles fused with additional membranes. Cyclical spiral membranes are seen that are reminiscent of the sarcolemmal inclusions found in human skeletal myopathy.

    The flight ability of Mhc10 mutants expressing MhcIFI-9b is normal.

    Adults expressing MhcIFI-9b in a Mhc10 mutant background show normal jumping ability.

    Flies expressing MhcEMB-9a in a Mhc10 mutant background are flightless.

    The jump ability of flies expressing MhcEMB-9a in a Mhc10 mutant background appears impaired.

    Compared with wild-type, the flight ability of Mhc10 mutants expressing Mhc15b is impaired. The flight ability of these flies declines more rapidly with age than that of controls.

    Compared with controls, Mhc10 mutant flies expressing Mhc15b display a reduced ability to jump.

    Electrophysiological responses of flight muscles in Mhc10 mutants expressing Mhc15b appear normal.

    Myofibrils of Mhc10 mutant flies expressing MhcIFI-7a show no differences in assembly or stability when compared to controls.

    Mhc10 mutant flies expressing MhcIFI-7a exhibit no impairment in flight or jump ability compared to controls.

    Expression of MhcEMB-7d in Mhc10 mutants allows normal myofibrillar assembly evidenced at 2 hours post-eclosion. By two days indirect flight muscle myofilaments do show some disruption.

    Transgenic Mhc10 mutant flies expressing MhcEMB-7d show impairment in jump ability and they are not able to fly.

    52% of homozygous adults have an upheld wing phenotype, 42% have their wings held down and 6% hold their wings in the normal position. The indirect flight muscle fibres appear normal. 4% of heterozygotes have an upheld wing phenotype. The indirect flight muscle fibres appear normal. 44% of Mhc10/+ ; MhcR57-24.Act88F/+ flies have their wings held down and 56% hold their wings in the normal position. The indirect flight muscle fibres appear normal. 76% of Mhc10/Mhc13 adults have an upheld wing phenotype, 24% have their wings held down and 0% hold their wings in the normal position. 39% of the indirect flight muscle fibres of mutant adults are hypercontracted, 61% show a partial hypercontraction phenotype.

    The myofibrillar ultrastructure in the indirect flight muscle of animals carrying MhcEMB-3b in a Mhc10 background is identical to wild type at the pupal stage. However, 2 days after eclosion, the filament packing is disrupted, and the normal rigid hexagonal arrangement of thick and thin filaments is disturbed. The myofibrils appear cracked and frayed when viewed longitudinally, because of gaps between thick and thin filaments and/or loss of thick and thin filaments. The phenotype becomes progressively worse with age. The myofibrillar ultrastructure in the indirect flight muscle of animals carrying MhcIFI-3a in a Mhc10 background is identical to wild type at the pupal stage. The myofilaments remain highly ordered and identical to wild type for at least two weeks following eclosion. Animals carrying Mhc+memb in a Mhc10 background show severe cracking and fraying of myofibrils in the indirect flight muscle. The basic sarcomere pattern is disrupted at 2 days after eclosion and 2 weeks after eclosion, myofibrils are no longer discernible.

    Indirect flight muscle (IFM) myofibrils expressing Mhc+memb in a Mhc10 background show ultrastructural deterioration, which begins soon after the age at which Drosophila normally begin using the IFMs. These flies cannot beat their wings. These flies can jump, but achieve much shorter differences than wild-type flies. Two day old flies expressing MhcEMB-IC in a Mhc10 background show some ultrastructural deterioration of the indirect flight muscle myofibrils. These flies cannot beat their wings. These flies can jump, but achieve much shorter differences than wild-type flies. Two day old flies expressing MhcIFI-EC in a Mhc10 background have indirect flight muscle myofibrils which are almost indistinguishable from wild type. These animals can fly.

    Flies carrying Mhcemb.ex18 in a Mhc10 mutant background exhibit normal-looking myofibrils at the pupal stage in the central regions, but myofilaments at the periphery are less organized. In young adults, the myofibrils are disorganised with cracking and fraying throughout. In 1-week old flies the myofibrils appear fairly well organised. The appear compacted and smaller in diameter, but there is no cracking or fraying at the periphery.

    Flies carrying Mhc+memb in a Mhc10 mutant background exhibit normal-looking myofibrils at the pupal stage. In young adults, the myofibrils are disorganised with cracking and fraying throughout. In 1-week old flies, the myofibrils are completely disorganised.

    Arrays of thin filaments and malformed Z-discs accumulate in the indirect flight muscles (IFMs) of Mhc10 flies, however, thick filaments are absent. Mhc10 flies expressing MhcR57-24.Act88F have thick filaments that are associated with myofibril-like structures in the IFMs. These myofibrils have Z-discs and occasional M-lines, however, sarcomere length and the length of the thick filaments is variable. The Z-discs are thicker than wild type. Many of the thick filaments are packed in a hexagonal manner and are frequently interdigitated with thin filaments. Often, six thin filaments surround each thick filament, as in wild type. However, the myofibrils are rarely circular in cross-section and show a variability in size compared to wild type. Mhc10 flies expressing MhcR21-1.Act88F have hollow thick filaments and myofibril-like structures in the IFMs. Hexagonal packing of the thick filaments with arrays of six thin filaments surrounding each thick filament is seen, as in wild type. Less rescue is seen than with MhcR57-24.Act88F.

    Homozygotes are flightless, one copy of Mhc+t41.9 improves flying ability but not to wild type levels. Homozygotes are also unable to jump, one copy of Mhc+t41.9 improves jumping ability.

    Mhc RNA, protein and thick filaments do not accumulate in the indirect flight muscles and jump muscles of the adult, and levels are reduced in the leg muscles.

    Indirect flight muscles accumulate little or no MHC, have no thick filaments, and show no organized myofibrils. All 32 TDT cells lack thick filaments and lack myofibril organization. Flies cannot jump. Leg muscles accumulate 55% normal amounts of MHC (O'Donnell, Collier, Mogami and Bernstein, 1989). homozygous viable

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    NOT suppressed by
    Enhancer of
    Statement
    Reference

    Mhc10 is an enhancer of abnormal flight | heat sensitive phenotype of Act57BUAS.cVa, Scer\GAL4Act88F.PB

    Suppressor of
    Statement
    Reference

    MhcR57-24.Act88F/Mhc10 is a suppressor of visible phenotype of up1

    Mhc[+]/Mhc10 is a suppressor | partially of visible phenotype of wupAhdp-2

    NOT Suppressor of
    Statement
    Reference

    Mhc10 is a non-suppressor of flightless | heat sensitive phenotype of Act57BM306L.UAS, Scer\GAL4Act88F.PB

    Mhc[+]/Mhc10 is a non-suppressor of flightless phenotype of wupAhdp-2

    Mhc[+]/Mhc10 is a non-suppressor of visible phenotype of up101

    Mhc[+]/Mhc10 is a non-suppressor of flightless phenotype of up101

    Phenotype Manifest In
    NOT suppressed by
    Suppressor of
    Statement
    Reference

    MhcR57-24.Act88F/Mhc10 is a suppressor of wing phenotype of up1

    MhcR57-24.Act88F/Mhc10 is a suppressor | partially of myosin filament & indirect flight muscle phenotype of up1

    MhcR57-24.Act88F/Mhc10 is a suppressor | partially of striated muscle thin filament & indirect flight muscle phenotype of up1

    MhcR57-24.Act88F/Mhc10 is a suppressor | partially of Z disc & indirect flight muscle phenotype of up1

    Mhc[+]/Mhc10 is a suppressor | partially of wing phenotype of wupAhdp-2

    NOT Suppressor of
    Statement
    Reference

    Mhc[+]/Mhc10 is a non-suppressor of wing phenotype of up101

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    The jump ability defects and the indirect flight muscle sarcomere defects observed in MhcK1728del/Mhc10 transheterozygotes are not suppressed by the expression of tnUAS.cDa under the control of Scer\GAL4Mef2.PR.

    Mhc10 completely suppresses the indirect flight muscle degeneration seen in newly eclosed flies expressing aretGD8699 under the control of Scer\GAL4Mef2.PR.

    Scer\GAL4Mef2.PR>Act57BK328Q.Scer\UAS; Mhc10/+ flies display a greater abundance of thoracic material and birefringent musculature indicating partial suppression of the indirect flight muscle (IFM) phenotype of Scer\GAL4Mef2.PR>Act57BK328Q.Scer\UAS.

    up1/Y ; Mhc10/Mhc+ ; MhcR57-24.Act88F flies have a normal wing posture and a normal indirect flight muscle morphology under polarised light. Ultrastructurally, sarcomere-like assemblies with Z-bands and thick and thin filaments are seen, although in most areas the filaments appear disorganised.

    Homozygous Mhc10 flies expressing MhcR57-24.Act88F completely restore indirect flight muscle fibre defects to a normal structural condition in heterozygous wupAhdp-3 flies. The thorax of wupAhdp-3/Y; Mhc10/+ flies have a small bunch of visible muscle mass, in contrast to wupAhdp-3 ; Mhc+/+ flies which have no visible indirect flight muscle. wupAhdp-3/Y; Mhc10/+ flies that express one copy of MhcR57-24.Act88F show a greater increase in muscle mass. This increase is greater still when flies express two copies of MhcR57-24.Act88F. Only in wupAhdp-3/Y; Mhc10/Mhc10 flies that express two copies of MhcR57-24.Act88F can actual myofibrillar structures be seen. In wupAhdp-3/Y; Mhc10/Mhc10; MhcR57-24.Act88F flies thick filaments, some thin filaments, isolated Z-discs and tiger-tails (formed by serially repeated Z-discs connected by short stretches of thin filaments) are readily visible but sarcomeric structures fail to assemble.

    The defects seen in wupAhdp-2/Y flies are partially suppressed by Mhc10/+; 49% of the double mutant adults have an upheld wing phenotype and 51% have their wings held down. 29% of the indirect flight muscle fibres are hypercontracted, 71% show a partial hypercontraction phenotype. The defects seen in wupAhdp-2/Y flies are almost completely suppressed by Mhc10/+ ; MhcR57-24.Act88F/+ - 13% of the double mutant adults have an upheld wing phenotype, 0% have their wings held down and 87% hold their wings in the normal position. 13% of the indirect flight muscle fibres show a partial hypercontraction phenotype and 87% are normal. The wing phenotypes of up101/Y flies are not suppressed by Mhc10/+, while in the double mutants, 80% of the indirect flight muscle fibres are hypercontracted, 20% show a partial hypercontraction phenotype.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Partially rescued by

    Mhc10 is partially rescued by MhcR21-1.Act88F

    Mhc10 is partially rescued by MhcR57-24.Act88F

    Mhc10 is partially rescued by Mhc+t41.9

    Not rescued by

    Mhc10 is not rescued by Mhc15b

    Comments

    MhcEMB-9c11d and MhcEMB-11d do not rescue flight or jump ability in a Mhc10 background.

    Mhc10 mutants expressing Mhc+t12.4 display normal jumping ability and ultrastructure.

    The flight ability of Mhc10 mutants expressing MhcIFI-9b is normal.

    Adults expressing MhcIFI-9b in a Mhc10 mutant background show normal jumping ability.

    Flies expressing MhcEMB-9a in a Mhc10 mutant background are flightless.

    The jump ability of flies expressing MhcEMB-9a in a Mhc10 mutant background appears impaired.

    Compared with wild-type, the flight ability of Mhc10 mutants expressing Mhc15b is impaired. The flight ability of these flies declines more rapidly with age than that of controls.

    Compared with controls, Mhc10 mutant flies expressing Mhc15b display a reduced ability to jump.

    Expression of Mhc15b in Mhc10 mutants results in myofibrils with generally wild-type structure. However, there are a variety of minor defects not observed in the control line including myofibrils with disrupted M lines and rough edges. The frequency and severity of defects vary among different insertion lines. Myofibril dimensions of Mhc10 mutants expressing Mhc15b differ from that of wild-type. The myofibril defects appear use-dependent as they are less frequent and less severe in newly eclosed flies than in older adults.

    Myofibrils of Mhc10 mutant flies expressing MhcIFI-7a show no differences in assembly or stability when compared to controls.

    Mhc10 mutant flies expressing MhcIFI-7a exhibit no impairment in flight or jump ability compared to controls.

    Expression of MhcEMB-7d in Mhc10 mutants allows normal myofibrillar assembly evidenced at 2 hours post-eclosion. By two days indirect flight muscle myofilaments do show some disruption.

    Transgenic Mhc10 mutant flies expressing MhcEMB-7d show impairment in jump ability and they are not able to fly.

    Flight ability is not rescued by either MhcR21-1.Act88F or MhcR57-24.Act88F in a Mhc10 background.

    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer

    Mogami.

    Comments
    Comments

    Transcripts in the indirect flight muscles (IFMs) and tergal depressor muscle of the trochanter (TDT) are missing. Overexpression of Mhc in the direct flight muscles may affect their function sufficiently to disrupt flight.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (2)
    References (47)