Some of Problems of Direction Finding of Ground-Based Radars Using Monopulse Location System Installed on Unmanned Aerial Vehicle.

Locating active radars in real environmental conditions is a very important and complex task. The efficiency of the direction finding (DF) of ground-based radars and other microwave emitters using unmanned aerial vehicles (UAV) is dependent on the parameters of applied devices for angle location of microwave emitters, and on the construction and modes of operation of the observed transmitting antenna systems. An additional factor having the influence on DF of the radar, when are used systems installed on the UAV, is the rotation of the antenna of a radar. The accuracy of estimation of direction of any microwave transmitter is determined by the terrain properties that surround the transmitter and the objects reflecting microwave signals. The exemplary shapes of the radar antenna patterns and the associated relationships with the probability of remotely detecting the radar and determining its bearings are described. The simulated patterns of the signals received at an emitter-locating device mounted on a UAV and the expected results of a monopulse DF based on these signals are presented. The novelty of this work is the analysis of the DF efficiency of radars in conditions where intense multi-path phenomena appear, and for various amplitudes and phases of the direct signal and multi-path signals that reach the UAV when assuming that so-called simple signals and linear frequency modulation (LFM) signals are transmitted by the radar. The primary focus is on multi-path phenomenon, which can make it difficult, but not entirely impossible, to detect activity and location of radar with a low-flying small UAV and using only monopulse techniques, that is, when only a single pulse emitted by a radar must be sufficient to DF of this radar. Direction of arrival (DOA) algorithms of signals in dense signal environment were not presented in the work, but relevant suggestions were made for the design of such algorithms.

Immunogold scanning electron microscopy can reveal the polysaccharide architecture of xylem cell walls.

Immunofluorescence microscopy (IFM) and immunogold transmission electron microscopy (TEM) are the two main techniques commonly used to detect polysaccharides in plant cell walls. Both are important in localizing cell wall polysaccharides, but both have major limitations, such as low resolution in IFM and restricted sample size for immunogold TEM. In this study, we have developed a robust technique that combines immunocytochemistry with scanning electron microscopy (SEM) to study cell wall polysaccharide architecture in xylem cells at high resolution over large areas of sample. Using multiple cell wall monoclonal antibodies (mAbs), this immunogold SEM technique reliably localized groups of hemicellulosic and pectic polysaccharides in the cell walls of five different xylem structures (vessel elements, fibers, axial and ray parenchyma cells, and tyloses). This demonstrates its important advantages over the other two methods for studying cell wall polysaccharide composition and distribution in these structures. In addition, it can show the three-dimensional distribution of a polysaccharide group in the vessel lateral wall and the polysaccharide components in the cell wall of developing tyloses. This technique, therefore, should be valuable for understanding the cell wall polysaccharide composition, architecture and functions of diverse cell types.

Characterization of specific allosteric effects of the Na+ channel ß1 subunit on the Nav1.4 isoform.

The mechanism of inactivation of mammalian voltage-gated Na+ channels involves transient interactions between intracellular domains resulting in direct pore occlusion by the IFM motif and concomitant extracellular interactions with the ß1 subunit. Navß1 subunits constitute single-pass transmembrane proteins that form protein-protein associations with pore-forming α subunits to allosterically modulate the Na+ influx into the cell during the action potential of every excitable cell in vertebrates. Here, we explored the role of the intracellular IFM motif of rNav1.4 (skeletal muscle isoform of the rat Na+ channel) on the α-ß1 functional interaction and showed for the first time that the modulation of ß1 is independent of the IFM motif. We found that: (1) Nav1.4 channels that lack the IFM inactivation particle can undergo a "C-type-like inactivation" albeit in an ultraslow gating mode; (2) ß1 can significantly accelerate the inactivation of Nav1.4 channels in the absence of the IFM motif. Previously, we identified two residues (T109 and N110) on the ß1 subunit that disrupt the α-ß1 allosteric modulation. We further characterized the electrophysiological effects of the double alanine substitution of these residues demonstrating that it decelerates inactivation and recovery from inactivation, abolishes the modulation of steady-state inactivation and induces a current rundown upon repetitive stimulation, thus causing a general loss of function. Our results contribute to delineating the process of the mammalian Na+ channel inactivation. These findings may be relevant to the design of pharmacological strategies, targeting ß subunits to treat pathologies associated to Na+ current dysfunction.

Subcellular location of the coupling protein TrwB and the role of its transmembrane domain.

Conjugation is the most important mechanism for horizontal gene transfer and it is the main responsible for the successful adaptation of bacteria to the environment. Conjugative plasmids are the DNA molecules transferred and a multiprotein system encoded by the conjugative plasmid itself is necessary. The high number of proteins involved in the process suggests that they should have a defined location in the cell and therefore, they should be recruited to that specific point. One of these proteins is the coupling protein that plays an essential role in bacterial conjugation. TrwB is the coupling protein of R388 plasmid that is divided in two domains: i) The N-terminal domain referred as transmembrane domain and ii) a large cytosolic domain that contains a nucleotide-binding motif similar to other ATPases. To investigate the role of these domains in the subcellular location of TrwB, we constructed two mutant proteins that comprised the transmembrane (TrwBTM) or the cytoplasmic (TrwBΔN70) domain of TrwB. By immunofluorescence and GFP-fusion proteins we demonstrate that TrwB and TrwBTM mutant protein were localized to the cell pole independently of the remaining R388 proteins. On the contrary, a soluble mutant protein (TrwBΔN70) was localized to the cytoplasm in the absence of R388 proteins. However, in the presence of other R388-encoded proteins, TrwBΔN70 localizes uniformly to the cell membrane, suggesting that interactions between the cytosolic domain of TrwB and other membrane proteins of R388 plasmid may happen. Our results suggest that the transmembrane domain of TrwB leads the protein to the cell pole.

Gly161 mutations associated with Primary Hyperoxaluria Type I induce the cytosolic aggregation and the intracellular degradation of the apo-form of alanine:glyoxylate aminotransferase.

Primary Hyperoxaluria Type I (PH1) is a severe rare disorder of metabolism due to inherited mutations on liver peroxisomal alanine:glyoxylate aminotransferase (AGT), a pyridoxal 5'-phosphate (PLP)-dependent enzyme whose deficiency causes the deposition of calcium oxalate crystals in the kidneys and urinary tract. PH1 is an extremely heterogeneous disease and there are more than 150 disease-causing mutations currently known, most of which are missense mutations. Moreover, the molecular mechanisms by which missense mutations lead to AGT deficiency span from structural, functional to subcellular localization defects. Gly161 is a highly conserved residue whose mutation to Arg, Cys or Ser is associated with PH1. Here we investigated the molecular bases of the AGT deficit caused by Gly161 mutations with expression studies in a mammalian cellular system paired with biochemical analyses on the purified recombinant proteins. Our results show that the mutations of Gly161 (i) strongly reduce the expression levels and the intracellular half-life of AGT, and (ii) make the protein in the apo-form prone to an electrostatically-driven aggregation in the cell cytosol. The coenzyme PLP, by shifting the equilibrium from the apo- to the holo-form, is able to reduce the aggregation propensity of the variants, thus partly decreasing the effect of the mutations. Altogether, these results shed light on the mechanistic details underlying the pathogenicity of Gly161 variants, thus expanding our knowledge of the enzymatic phenotypes leading to AGT deficiency.

Effect of nickel oxide nanoparticles on bioethanol production by Pichia kudriavzveii IFM 53048 using banana peel waste substrate.

The use of nanomaterials in bioethanol production is promising and on the increase. In this report, the effect of nickel oxide nanoparticles (NiO NPs) on bioethanol production in the presence of a novel yeast strain, Pichia kudriavzveii IFM 53048 isolated from banana wastes was investigated. The hot percolation method was employed for the green synthesis of NiO NPs. The logistic and modified Gompertz kinetic models employed in this study showed a 0.99 coefficient of determination (R2) on cell growth, and substrate utilization on the initial rate data plot which indicate that these model were best suited for bioethanol production studies. As a result, 99.95% of the substrate was utilized to give 0.23 g/L/h-1 bioethanol productivity, and 51.28% fermentation efficiency, respectively. At 0.01 wt% of NiO NPs, maximum production was achieved with 0.27 g/g bioethanol yield. Meanwhile, 0.78 h-1 maximum specific growth rate (µmax) of the microorganism, 3.77 g/L bioethanol concentration (Pm), 0.49 g/L/h production rate (rp.m), and 2.43 h production lag time (tL) were obtained when 0.01 wt% of NiO NPs were used during the bioethanol production process. However, a decrease in bioethanol concentrations occurred at ≥0.02 wt% of NiO NPs. The incorporation of NiO NPs in the simultaneous saccharification and fermentation (SSF) process improved the production of bioethanol by 1.90 fold using banana peel wastes as substrate. These revealed NiO NPs could serve as a suitable biocatalyst in the green production of bioethanol from banana peel waste materials.

Rab11 rescues muscle degeneration and synaptic morphology in the park13/+ Parkinson model of Drosophila melanogaster.

Mutation in parkin and pink1 is associated with Parkinson's disease (PD), the most common movement disorder characterized by muscular dysfunction. In a previous study, we observed that Rab11, a member of the small Ras GTPase family, regulates the mitophagy pathway mediated by Parkin and Pink1 in the larval brain of the Drosophila PD model. Here, we describe that the expression and interaction of Rab11 in the PD model of Drosophila is highly conserved across different phylogenic groups. The loss of function in these two proteins, i.e., Parkin and Pink1, leads to mitochondrial aggregation. Rab11 loss of function results in muscle degeneration, movement disorder and synaptic morphological defects. We report that overexpression of Rab11 in park13 heterozygous mutant improves muscle and synaptic organization by reducing mitochondrial aggregations and improving cytoskeleton structural organization. We also show the functional relationship between Rab11 and Brp, apre-synaptic scaffolding protein, required for synaptic neurotransmission. Using park13 heterozygous mutant and pink1RNAi lines, we showed reduced expression of Brp and consequently, there were synaptic dysfunctions including impaired synaptic transmission, decreased bouton size, increase in the bouton numbers, and the length of axonal innervations at the larval neuromuscular junction (NMJ). These synaptic alterations were rescued with the over-expression of Rab11 in the park13 heterozygous mutants. In conclusion, this work emphasizes the importance of Rab11 in rescuing muscle degeneration, movement dysfunction and synaptic morphology by preserving mitochondrial function in the PD model of Drosophila.

First case report of cerebral abscess from Nocardia terpenica and literature review.

Nocardia is a Gram-positive weakly acid-fast bacterium that is ubiquitous in the environment. It represents a rare cause of infection in humans and typically causes pulmonary, cutaneous, or central nervous system (CNS) infections. CNS nocardiosis has very poor prognosis, especially in immunocompromised hosts. Nocardia terpenica is a species of Nocardia consisting of two strains that were reclassified from Nocardia brasiliensis in 2007. We report the second case of CNS Nocardia terpenica infection, and the first case of cerebral abscess from Nocardia terpenica. This report raises the index of suspicion for nocardiosis when evaluating contrast-enhancing CNS lesions, points out the capability of this species for CNS spread, and shares our experience regarding management and prognosis.

Differential Effects of Reperfusion on Cardiac Mitochondrial Subpopulations in a Preclinical Porcine Model of Acute Myocardial Infarction.

Acute myocardial infarction (AMI) leads to localized cardiac ischemia and can be fatal if untreated. Despite being treatable, the threat of ischemia-reperfusion (IR) injury remains high. Mitochondria are central to both propagation and mitigation of IR injury, and cardiac mitochondria are categorized into two major subtypes-subsarcolemmal and interfibrillar mitochondria (SSM and IFM, respectively). We hypothesized that, in our pre-clinical porcine model of AMI, SSM and IFM are differentially affected by reperfusion. AMI was induced in female pigs by balloon occlusion of the left anterior descending artery for 45 min, followed by 4 h of reperfusion. At the end of reperfusion, animals were euthanized. Cardiac SSM and IFM from the affected ischemic area and a nearby non-ischemic area were isolated to compare mitochondrial function using substrates targeting mitochondrial electron transport chain complexes I and II. Despite detecting overall significant differences in mitochondrial function including yield, mitochondrial S3 and S4 respirations, and calcium retention, consistent individual functional differences in the two mitochondrial subpopulations were not observed, both between the two mitochondrial subtypes, as well as between the ischemic and non-ischemic tissue. Nonetheless, this study describes the mitochondrial subtype response within the initial few hours of reperfusion in a clinically relevant model of AMI, which provides valuable information needed to develop novel mitochondrially targeted therapies for AMI.

Regular Exercise Rescues Heart Function Defects and Shortens the Lifespan of Drosophila Caused by dMnM Downregulation.

Although studies have shown that myomesin 2 (MYOM2) mutations can lead to hypertrophic cardiomyopathy (HCM), a common cardiovascular disease that has a serious impact on human life, the effect of MYOM2 on cardiac function and lifespan in humans is unknown. In this study, dMnM (MYOM2 homologs) knockdown in cardiomyocytes resulted in diastolic cardiac defects (diastolic dysfunction and arrhythmias) and increased cardiac oxidative stress. Furthermore, the knockdown of dMnM in indirect flight muscle (IFM) reduced climbing ability and shortened lifespan. However, regular exercise significantly ameliorated diastolic cardiac dysfunction, arrhythmias, and oxidative stress triggered by dMnM knockdown in cardiac myocytes and also reversed the reduction in climbing ability and shortening of lifespan caused by dMnM knockdown in Drosophila IFM. In conclusion, these results suggest that Drosophila cardiomyocyte dMnM knockdown leads to cardiac functional defects, while dMnM knockdown in IFM affects climbing ability and lifespan. Furthermore, regular exercise effectively upregulates cardiomyocyte dMnM expression levels and ameliorates cardiac functional defects caused by Drosophila cardiomyocyte dMnM knockdown by increasing cardiac antioxidant capacity. Importantly, regular exercise ameliorates the shortened lifespan caused by dMnM knockdown in IFM.

When the Gates Swing Open Only: Arrhythmia Mutations That Target the Fast Inactivation Gate of Nav1.5.

Nav1.5 is the main voltage-gated sodium channel found in cardiac muscle, where it facilitates the fast influx of Na+ ions across the cell membrane, resulting in the fast depolarization phase-phase 0 of the cardiac action potential. As a result, it plays a major role in determining the amplitude and the upstroke velocity of the cardiac impulse. Quantitively, cardiac sodium channel activates in less than a millisecond to trigger the cardiac action potential and inactivates within 2-3 ms to facilitate repolarization and return to the resting state in preparation for firing the next action potential. Missense mutations in the gene that encodes Nav1.5 (SCN5A), change these time constants which leads to a wide spectrum of cardiac diseases ranging from long QT syndrome type 3 (LQT3) to sudden cardiac death. In this mini-review I will focus on the missense mutations in the inactivation gate of Nav1.5 that results in arrhythmia, attempting to correlate the location of the missense mutation to their specific phenotype.

Large-Size Suspended Mono-Layer Graphene Film Transfer Based on the Inverted Floating Method.

Suspended graphene can perfectly present the excellent material properties of graphene, which has a good application prospect in graphene sensors. The existing suspended graphene pressure sensor has several problems that need to be solved, one of which is the fabrication of a suspended sample. It is still very difficult to obtain large-size suspended graphene films with a high integrity that are defect-free. Based on the simulation and analysis of the kinetic process of the traditional suspended graphene release process, a novel setup for large-size suspended graphene release was designed based on the inverted floating method (IFM). The success rate of the single-layer suspended graphene with a diameter of 200 µm transferred on a stainless-steel substrate was close to 50%, which is greatly improved compared with the traditional impregnation method. The effects of the defects and burrs around the substrate cavity on the stress concentration of graphene transfer explain why the transfer success rate of large-size suspended graphene is not high. This research lays the foundation for providing large-size suspended graphene films in the area of graphene high-precision sensors.

Superresolution Microscopy of Drosophila Indirect Flight Muscle Sarcomeres.

Sarcomeres are extremely highly ordered macromolecular assemblies where proper structural organization is an absolute prerequisite to the functionality of these contractile units. Despite the wealth of information collected, the exact spatial arrangement of many of the H-zone and Z-disk proteins remained unknown. Recently, we developed a powerful nanoscopic approach to localize the sarcomeric protein components with a resolution well below the diffraction limit. The ease of sample preparation and the near crystalline structure of the Drosophila flight muscle sarcomeres make them ideally suitable for single molecule localization microscopy and structure averaging. Our approach allowed us to determine the position of dozens of H-zone and Z-disk proteins with a quasi-molecular, ~5-10 nm localization precision. The protocol described below provides an easy and reproducible method to prepare individual myofibrils for dSTORM imaging. In addition, it includes an in-depth description of a custom made and freely available software toolbox to process and quantitatively analyze the raw localization data.

Assessing Mitochondrial Bioenergetics in Isolated Mitochondria from Mouse Heart Tissues Using Oroboros 2k-Oxygraph.

In this chapter, we describe detailed protocols for measuring high-resolution respirometry on mitochondria extracted from adult whole mouse heart using the Oroboros 2k-Oxygraph system. The method provides detailed procedures for the preparation of mitochondria and measurement of high-resolution respirometry in response to various respiration inhibitions. The method described in this chapter could discern the different respiration rate on mitochondria extracted from two spatially distinct mitochondrial subpopulations, subsarcolemmal mitochondria (SSM) and intermyofibrillar mitochondria (IFM). These approaches can easily be translated to other cells and tissues.

Intervention fidelity monitoring of Urban Zen Integrative Therapy (UZIT) for persons with pulmonary hypertension.

BACKGROUND: Systematic and consistent dose delivery is critical in intervention research. Few studies testing complementary health approach (CHA) interventions describe intervention fidelity monitoring (IFM) and measurement. OBJECTIVE: To describe methodological processes in establishing and measuring consistent dose, delivery, and duration of a multi-component CHA intervention. METHODS: Adults with pulmonary hypertension received six weekly, 1-hour Urban Zen Integrative Therapy (UZIT) sessions. A total of 78 sessions were delivered and 33% of these sessions were audited. Intervention dose (time allocated to each component), intervention consistency (protocol adherence audits), and intervention delivery (performance and sequence of components) were captured using remote video observation and review of the recorded video. IFM audits were performed at the beginning (n = 16), middle (n = 5), and end (n = 5) of the study. RESULTS: UZIT interventionists adhered to the intervention protocol (99.3%) throughout the study period. Interventionists delivered UZIT components within the prescribed timeframe: 1) Beginning: gentle body movement (18.9 ± 5.8 min.), restorative pose with guided body awareness meditation (21.3 ± 2.7 min.), and Reiki (22.8 ± 3.1 min.); 2) Middle: gentle body movement (15.9 ± 1.5 min.), pose/body awareness meditation (30.1 ± 6.5 min.), and Reiki (30.1 ± 7.0 min.); 3) End: gentle body movement (18.1 ± 3.6 min.), pose/body awareness meditation (35.3 ± 6.4 min.), and Reiki (34.5 ± 7.0 min.). Essential oil inhalation was delivered during UZIT sessions 100% of the time. Interventionists adhered to treatment delivery behaviors throughout the study period: beginning (98.86%), middle (100%), and end (100%). DISCUSSION: In this pilot study, we demonstrated that the dose, consistency, and delivery of multi-component CHA therapy can be standardized and monitored to ensure intervention fidelity.

Interfascicular matrix-mediated transverse deformation and sliding of discontinuous tendon subcomponents control the viscoelasticity and failure of tendons.

In the present article, we investigated the sliding of discontinuous tendon subcomponents and the variation of nonhomogeneous deformation in the human Achilles tendon (AT) over time using uniaxial tensile and relaxation tests. The deformation and the resulting strain distribution under uniaxial tension are examined using a vision-based 3-D digital image correlation (DIC) system, which allows estimation of the strain field in the axial and lateral directions. Relaxation test under B-mode ultrasound imaging with the use of DIC method provides information about the local strain variation over time in the axial and anteroposterior directions. The observed nonhomogeneous deformation, a result from the twisted structure of the tendon, shows both compressive and tensile transverse strains that can generate interfascicular matrix (IFM) failure and initiate water accumulation in the course of tendinopathy. Moreover, using B-mode elastography with the DIC method, we have observed areas of low stiffness when the strain values exceed the strength limits, and this could correspond to IFM carrying the load between discontinuous tendon subcomponents. Thus, IFM carrying complex multiscale stresses may be responsible for the strength and viscoelastic properties of the AT. The results presented here reveal a new pathomechanism of AT failure. This could be useful in further studies on tendinopathy as well as effective planning of the AT therapy.

Mouse cardiac mitochondria do not separate in subsarcolemmal and interfibrillar subpopulations.

Cardiomyocytes consist of longitudinally oriented myofibril bundles with a misaligned composition caused by the uneven contours of the intercalated discs. The cytoplasmic space harbors the organelles, including mitochondria. This study investigated whether cardiomyocytes contain spatially and ultrastructurally discrete pools of mitochondria that can be separated for structurally and functionally appraisal in (patho)physiology. Transmission electron microscopy disclosed continuous transitions of mitochondria without attributable characteristics from beneath the sarcolemma directly into the barrier-free cytoplasmic space between myofibrils. The various shapes and sizes of mitochondria are formed by myofibril positioning and the space available independent of their localization within the cardiomyocytes. Furthermore, the established enzymatic isolation procedure including proteinase treatment resulted in loss of mitochondrial proteins, as evidenced by immunogold labeling of Connexin43 in situ, a postulated marker for distinguishing mitochondrial subpopulations. Moreover, mitochondrial ATP produced in those mitochondria was not different. These findings preclude a spatial and ultrastructural grading of cardiac mitochondria and their distinct separation and classification in subsarcolemmal and interfibrillar subpopulations.

Nagarse treatment of cardiac subsarcolemmal and interfibrillar mitochondria leads to artefacts in mitochondrial protein quantification.

INTRODUCTION: In the heart, subsarcolemmal (SSM), interfibrillar (IFM) and perinuclear mitochondria represent three subtypes of mitochondria. The most commonly used protease during IFM isolation is the nagarse, however, its effect on the detection of mitochondrial proteins is still unclear. Therefore, we investigated whether nagarse treatment influences the quantification of mitochondrial proteins. METHODS: SSM and IFM were isolated from hearts of mice and rats. During IFM isolation, nagarse activity was either stopped by centrifugation (common protocol, IFM+N) or inhibited by phenylmethylsulfonyl fluoride (PMSF, IFM+N+I). The amounts of proteins located in different mitochondrial compartments (outer membrane: mitofusin 1 (MFN1) and 2 (MFN2); intermembrane space: p66shc; inner membrane (connexin 43 (Cx43)), and of protein deglycase DJ-1 were determined by Western blot. RESULTS: MFN2 and Cx43 were found predominantly in SSM isolated from mouse and rat hearts. MFN1 and p66shc were present in similar amounts in SSM and IFM+N, whereas the level of DJ-1 was higher in IFM+N compared to SSM. In IFM+N+I samples from mice, the amount of MFN2, but not that of Cx43 increased. Nagarse or nagarse inhibition by PMSF had no effect on oxygen consumption of SSM or IFM. DISCUSSION: Whereas the use of the common protocol indicates the localization of MFN2 predominantly in SSM, the inhibition of nagarse by PMSF increases the signal of MFN2 in IFM to that of in SSM, indicating an underestimation of MFN2 in IFM. Therefore, protease sensitivity should be considered when assessing distribution of mitochondrial proteins using nagarse-based isolation.

Engineering metabolic pathways in Amycolatopsis japonicum for the optimization of the precursor supply for heterologous brasilicardin congeners production.

The isoprenoid brasilicardin A is a promising immunosuppressant compound with a unique mode of action, high potency and reduced toxicity compared to today's standard drugs. However, production of brasilicardin has been hampered since the producer strain Nocardia terpenica IFM0406 synthesizes brasilicardin in only low amounts and is a biosafety level 2 organism. Previously, we were able to heterologously express the brasilicardin gene cluster in the nocardioform actinomycete Amycolatopsis japonicum. Four brasilicardin congeners, intermediates of the BraA biosynthesis, were produced. Since chemical synthesis of the brasilicardin core structure has remained elusive we intended to produce high amounts of the brasilicardin backbone for semi synthesis and derivatization. Therefore, we used a metabolic engineering approach to increase heterologous production of brasilicardin in A. japonicum. Simultaneous heterologous expression of genes encoding the MVA pathway and expression of diterpenoid specific prenyltransferases were used to increase the provision of the isoprenoid precursor isopentenyl diphosphate (IPP) and to channel the precursor into the direction of diterpenoid biosynthesis. Both approaches contributed to an elevated heterologous production of the brasilicardin backbone, which can now be used as a starting point for semi synthesis of new brasilicardin congeners with better properties.

Transcriptome analysis of IFM-specific actin and myosin nulls in Drosophila melanogaster unravels lesion-specific expression blueprints across muscle mutations.

Muscle contraction is a highly fine-tuned process that requires the precise and timely construction of large protein sub-assemblies to form sarcomeres. Mutations in many genes encoding constituent proteins of this macromolecular machine result in defective functioning of the muscle tissue. However, the pathways underlying muscle degeneration, and manifestation of myopathy phenotypes are not well understood. In this study, we explored transcriptional alterations that ensue from the absence of the two major muscle proteins - myosin and actin - using the Drosophila indirect flight muscles. Our aim was to understand how the muscle tissue responds as a whole to the absence of either of the major scaffold proteins, whether the responses are generic to the tissue; or unique to the thick versus thin filament systems. Our results indicated that muscles respond by altering gene transcriptional levels in multiple systems active in muscle remodelling, protein degradation and heat shock responses. However, there were some responses that were filament-specific signatures of muscle degeneration, like immune responses, metabolic alterations and alterations in expression of muscle structural genes and mitochondrial ribosomal genes. These general and filament-specific changes in gene expression may be of relevance to human myopathies.