Ifm(2)2 is a myosin heavy chain allele that disrupts myofibrillar assembly only in the indirect flight muscle of Drosophila melanogaster.

Chun, Miyoung; Falkenthal, Scott

doi:10.1083/jcb.107.6.2613

Cited by 57 publications

(37 citation statements)

References 38 publications

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“…The aberrant mitochondrial orientation we observed may be a consequence of the overall disturbance in the sarcomere packing and organization. The murine cardiac sarcomeric defects are similar to those observed in the IFM of Drosophila heterozygous for the null myosin heavy chain allele MHC36B Ifm2 (2) (8,24). In the insect's IFM, thin filament assembly appeared overtly normal but the sarcomere was severely disorganized.…”

Section: Discussionsupporting

confidence: 55%

Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart.

Jones¹,

Grupp²,

Doetschman³

et al. 1996

J. Clin. Invest.

189

140

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The ␣ -myosin heavy chain ( ␣ -MyHC) is the major contractile protein expressed in the myocardium of adult mice. We have produced mice carrying a null mutation of ␣ -MyHC by homologous recombination in murine ES cells. Homozygous null animals die between 11 and 12 d in utero of gross heart defects, while ␣ -MyHC ϩ / Ϫ heterozygotes survive and appear externally normal. The presence of a single functional ␣ -MyHC ϩ allele in heterozygous animals results in reduced levels of the transcript and protein as well as fibrosis and alterations in sarcomeric structure. Examination of heart function using a working heart preparation revealed severe impairment of both contractility and relaxation in a subset of the ␣ -MyHC ϩ / Ϫ animals. Thus, two ␣ -MyHC ϩ alleles are necessary for normal cardiac development, and hemizygosity for the normal allele can result in altered cardiac function. ( J. Clin. Invest. 1996Invest. . 98:1906Invest. -1917

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Section: Discussionsupporting

confidence: 55%

Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart.

Jones¹,

Grupp²,

Doetschman³

et al. 1996

J. Clin. Invest.

189

140

View full text Add to dashboard Cite

show abstract

“…Some of the myosin heavy chain and actin mutations are null, i.e., they specify no detectable protein. The Mhc36B mutation Ifm(2)2 is a flight musclespecific null allele that eliminates all myosin heavy chain mRNA and protein from these fibers (Mogami and Hotta 1981;Chun and Falkenthal 1988;C.J. Beall et al, unpubl.…”

mentioning

confidence: 99%

Genetic dissection of Drosophila myofibril formation: effects of actin and myosin heavy chain null alleles.

Beall¹,

Sepanski²,

Fyrberg³

1989

Genes Dev.

151

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We used null mutations of Drosophila actin and myosin genes to investigate two aspects of myofibril assembly.First, we eliminated all actin or myosin in flight muscles to evaluate contributions of thick and thin filaments to sarcomere formation. Results demonstrate that thick and thin filament arrays can assemble independently but that both are essential for sarcomeric order and periodicity. Second, we examined how filament stoichiometry affects myofibril assembly. We find that heterozygotes for actin (Act88F) or myosin heavy chain (Mhc36B) null alleles have complex myofibrillar defects, whereas Mhc36B-/+ ; Act88F-/+ double heterozygotes have nearly normal myofibrils. These results imply that most defects observed in single heterozygotes are due to filament imbalances, not deficits, and suggest that thick and thin filament interactions regulate myofibrillar growth and alignment.

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“…A second class of mutations acts upon a limited number of muscles, including the indirect flight muscles (Chun and Falkenthal, 1988;Collier et al, 1990;Kronert et al, 1991Kronert et al, , 1994O'Donnell et al, 1989). These homozygous-viable mutations affect alternative exons that are used only in these specific muscle types.…”

Section: Insights Provided By Flightlessmentioning

confidence: 99%

Determining structure/function relationships for sarcomeric myosin heavy chain by genetic and transgenic manipulation of Drosophila

Swank

Wells

Kronert

et al. 2000

Microsc. Res. Tech.

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Ifm(2)2 is a myosin heavy chain allele that disrupts myofibrillar assembly only in the indirect flight muscle of Drosophila melanogaster.

Abstract: Abstract. Using a combination of molecular and genetic techniques we demonstrate that Ifm(2)2 is an

Cited by 57 publications

References 38 publications

Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart.

Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart.

Genetic dissection of Drosophila myofibril formation: effects of actin and myosin heavy chain null alleles.

Determining structure/function relationships for sarcomeric myosin heavy chain by genetic and transgenic manipulation of Drosophila

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