scholarly journals 3D Mitochondrial Ultrastructure of Drosophila Indirect Flight Muscle Revealed by Serial-section Electron Tomography

10.3791/56567 ◽  
2017 ◽  
Author(s):  
Yi-fan Jiang ◽  
Hsiang-ling Lin ◽  
Chi-yu Fu
Keyword(s):  
Serial Section ◽  
Flight Muscle ◽  
Electron Tomography ◽  
Indirect Flight Muscle ◽  
Mitochondrial Ultrastructure ◽  
Section Electron

scholarly journals Semi‐automatic stitching of filamentous structures in image stacks from serial‐section electron tomography

2021 ◽  
Author(s):  
Norbert Lindow ◽  
Florian N. Brünig ◽  
Vincent J. Dercksen ◽  
Gunar Fabig ◽  
Robert Kiewisz ◽  
...  
Keyword(s):  
Serial Section ◽  
Electron Tomography ◽  
Section Electron

Serial Section Electron Tomography: A Method for Three-Dimensional Reconstruction of Large Structures

NeuroImage ◽  
1994 ◽  
Vol 1 (3) ◽  
pp. 230-243 ◽  
Author(s):  
Gabriel E. Soto ◽  
Stephen J. Young ◽  
Maryann E. Martone ◽  
Thomas J. Deerinck ◽  
Stephan Lamont ◽  
...  
Keyword(s):  
Serial Section ◽  
Electron Tomography ◽  
Three Dimensional ◽  
Three Dimensional Reconstruction ◽  
Large Structures ◽  
Dimensional Reconstruction ◽  
Section Electron

Normal Synaptonemal Complex and Abnormal Recombination Nodules in Two Alleles of the Drosophila Meiotic Mutant mei-W68

Genetics ◽  
2003 ◽  
Vol 163 (4) ◽  
pp. 1337-1356 ◽  
Author(s):  
Adelaide T C Carpenter
Keyword(s):  
Electron Microscopy ◽  
Synaptonemal Complex ◽  
High Frequency ◽  
Serial Section ◽  
The Other ◽  
Wild Type ◽  
Recombination Nodules ◽  
Section Electron ◽  
Serial Section Electron Microscopy ◽  
Section Electron Microscopy

Abstract The meiotic phenotypes of two mutant alleles of the mei-W68 gene, 1 and L1, were studied by genetics and by serial-section electron microscopy. Despite no or reduced exchange, both mutant alleles have normal synaptonemal complex. However, neither has any early recombination nodules; instead, both exhibit high numbers of very long (up to 2 μm) structures here named “noodles.” These are hypothesized to be formed by the unchecked extension of identical but much shorter structures ephemerally seen in wild type, which may be precursors of early recombination nodules. Although the mei-W68L1 allele is identical to the mei-W681 allele in both the absence of early recombination nodules and a high frequency of noodles (i.e., it is amorphic for the noodle phene), it is hypomorphic in its effects on exchange and late recombination nodules. The differential effects of this allele on early and late recombination nodules are consistent with the hypothesis that Drosophila females have two separate recombination pathways—one for simple gene conversion, the other for exchange.

scholarly journals The Drosophila indirect flight muscle myosin heavy chain isoform is insufficient to transform the jump muscle into a highly stretch-activated muscle type

2017 ◽  
Vol 312 (2) ◽  
pp. C111-C118 ◽  
Author(s):  
Cuiping Zhao ◽  
Douglas M. Swank
Keyword(s):  
Power Generation ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Flight Muscle ◽  
Fold Increase ◽  
Isometric Tension ◽  
Indirect Flight Muscle ◽  
Muscle Type ◽  
Myosin Heavy Chain Isoform ◽  
Muscle Types

Stretch activation (SA) is a delayed increase in force that enables high power and efficiency from a cyclically contracting muscle. SA exists in various degrees in almost all muscle types. In Drosophila, the indirect flight muscle (IFM) displays exceptionally high SA force production ( FSA), whereas the jump muscle produces only minimal FSA. We previously found that expressing an embryonic (EMB) myosin heavy chain (MHC) isoform in the jump muscle transforms it into a moderately SA muscle type and enables positive cyclical power generation. To investigate whether variation in MHC isoforms is sufficient to produce even higher FSA, we substituted the IFM MHC isoform (IFI) into the jump muscle. Surprisingly, we found that IFI only caused a 1.7-fold increase in FSA, less than half the increase previously observed with EMB, and only at a high Pi concentration, 16 mM. This IFI-induced FSA is much less than what occurs in IFM, relative to isometric tension, and did not enable positive cyclical power generation by the jump muscle. Both isometric tension and FSA of control fibers decreased with increasing Pi concentration. However, for IFI-expressing fibers, only isometric tension decreased. The rate of FSA generation was ~1.5-fold faster for IFI fibers than control fibers, and both rates were Pi dependent. We conclude that MHC isoforms can alter FSA and hence cyclical power generation but that isoforms can only endow a muscle type with moderate FSA. Highly SA muscle types, such as IFM, likely use a different or additional mechanism.

Isolation and characterization of flightless mutants in Drosophila melanogaster

Development ◽  
1978 ◽  
Vol 45 (1) ◽  
pp. 123-143
Author(s):  
Takao Koana ◽  
Yoshiki Hotta
Keyword(s):  
Drosophila Melanogaster ◽  
Flight Muscle ◽  
Chromosomal Mapping ◽  
Indirect Flight Muscle ◽  
Mapping Technique ◽  
Isolation And Characterization ◽  
Genetic Mosaic ◽  
Column Type ◽  
Muscle Genes ◽  
Development And Differentiation

Since animal behaviour is executed through neuronal circuits including sensory receptors and muscle, genes vital for their development and differentiation must be found among mutants having behavioural anomaly. After mutagenesis with ethyl methanesulphonate (EMS), we screened for X-linked flightless mutants of Drosophila melanogaster by using a column-type flight tester. Approximately 104 individuals were screened and 21 mutant genes were isolated. Chromosomal mapping and complementation experiments revealed that they belong to 15 cistrons randomly located on X chromosome, three cistrons having more than two alleles. Two of the isolated mutants (AtO2 and AtH, which are recessive both behaviourally and morphologically) were analysed with the mosaic fate mapping technique, and both were found to have their primary foci in mesodermal region of blastoderm, suggesting that the genes exert their primary effect in indirect flight muscle. Electronmicroscopic studies on the muscles from four alleles of the AtO2 cistron revealed an abnormality in myofibrillar arrangement. A possible deficit within Z-band components is discussed in relation to wings-up B mutants. The indirect flight muscle of AltH was also examined, and it was found that sarcomere length and diameter of myofibrils were abnormal. It was postulated that a possible factor which controls size of myofibrils is defective in this mutant. These examples indicate the advantage of combining ultrastructural examination with genetic mosaic mapping technique.

scholarly journals Molecular and ultrastructural defects in a Drosophila myosin heavy chain mutant: differential effects on muscle function produced by similar thick filament abnormalities.

1988 ◽  
Vol 107 (6) ◽  
pp. 2601-2612 ◽  
Author(s):  
P T O'Donnell ◽  
S I Bernstein
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Muscle Function ◽  
Flight Muscle ◽  
Thick Filament ◽  
Differential Sensitivity ◽  
Indirect Flight Muscle ◽  
Molecular Defect ◽  
Thick Filaments ◽  
Nuclease Mapping

We have determined the molecular defect of the Drosophila melanogaster myosin heavy chain (MHC) mutation Mhc and the mutation's effect on indirect flight muscle, jump muscle, and larval intersegmental muscle. We show that the Mhc1 mutation is essentially a null allele which results in the dominant-flightless and recessive-lethal phenotypes associated with this mutant (Mogami, K., P. T. O'Donnell, S. I. Bernstein, T. R. F. Wright, C. P. Emerson, Jr. 1986. Proc. Natl. Acad. Sci. USA. 83:1393-1397). The mutation is a 101-bp deletion in the MHC gene which removes most of exon 5 and the intron that precedes it. S1 nuclease mapping indicates that mutant transcripts follow two alternative processing pathways. Both pathways result in the production of mature transcripts with altered reading frames, apparently yielding unstable, truncated MHC proteins. Interestingly, the preferred splicing pathway uses the more distal of two available splice donor sites. We present the first ultrastrutural characterization of a completely MHC-null muscle and show that it lacks any discernable thick filaments. Sarcomeres in these muscles are completely disorganized suggesting that thick filaments play a critical role in sarcomere assembly. To understand why the Mhc1 mutation severely disrupts indirect flight muscle and jump muscle function in heterozygotes, but does not seriously affect the function of other muscle types, we examined the muscle ultrastructure of Mhc1/+ heterozygotes. We find that these organisms have a nearly 50% reduction in the number of thick filaments in indirect flight muscle, jump muscle, and larval intersegmental muscle. In addition, aberrantly shaped thick filaments are common in the jump muscle and larval intersegmental muscle. We suggest that the differential sensitivity of muscle function to the Mhc1 mutation is a consequence of the unique myofilament arrays in each of these muscles. The highly variable myofilament array of larval intersegmental muscle makes its function relatively insensitive to changes in thick filament number and morphology. Conversely, the rigid double hexagonal lattice of the indirect flight muscle, and the organized lattice of the jump muscle cannot be perturbed without interfering with the specialized and evolutionarily more complex functions they perform.

Functional and ultrastructural effects of a missense mutation in the indirect flight muscle-specific actin gene of Drosophila melanogaster

1991 ◽  
Vol 222 (4) ◽  
pp. 963-982 ◽  
Author(s):  
John Sparrow ◽  
Mary Reedy ◽  
Elizabeth Ball ◽  
Vassilis Kyrtatas ◽  
Justin Molloy ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Missense Mutation ◽  
Flight Muscle ◽  
Indirect Flight Muscle ◽  
Actin Gene
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