Zebrafish Muscle Research Articles

High-resolution polarization-sensitive optical coherence tomography for zebrafish muscle imaging.

Zebrafish are an important animal model, whose structure and function information can be used to study development, pathologic changes and genetic mutations. However, limited by the penetration depth, the available optical methods are difficult to image the whole-body zebrafish in juvenile and adult stages. Based on a home-made high-resolution polarization-sensitive optical coherence tomography (PS-OCT) system, we finished in vivo volumetric imaging for zebrafish, and various muscles can be clearly discerned by scanning from dorsal, ventral, and lateral directions. Besides structure information, polarization properties extracted from PS-OCT images provide abundant function information to distinguish different muscles. Furthermore, we found local retardation and local optic axis of zebrafish muscle are related to their composition and fiber orientation. We think high-resolution PS-OCT will be a promising tool in studying myopathy models of zebrafish.

Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish

Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. Carnitine-depleted male Nile tilapia (initial weight: 4.29±0.12g; 3 mo old) were established by feeding them with mildronate diets (1000mg/kg/d) for 6wk. Zebrafish deficient in the carnitine palmitoyltransferase 1b gene (cpt1b) were produced by using CRISPR/Cas9 gene-editing technology, and their males (154±3.52mg; 3 mo old) were used for experiments. Normal Nile tilapia and wildtype zebrafish were used as controls. We assessed nutrient metabolism and energy homeostasis-related biochemical and molecular parameters, and performed 14C-labeled nutrient tracking and transcriptomic analyses. The mitochondrial FAO decreased by 33.1-88.9% (liver) and 55.6-68.8% (muscle) in carnitine-depleted Nile tilapia and cpt1b-deficient zebrafish compared with their controls (P <0.05). Notably, glucose oxidation and muscle protein deposition increased by 20.5-24.4% and 6.40-8.54%, respectively, in the 2 fish models compared with their corresponding controls (P <0.05). Accordingly, the adenosine 5'-monophosphate-activated protein kinase/protein kinase B-mechanistic target of rapamycin (AMPK/AKT-mTOR) signaling was significantly activated in the 2 fish models with inhibited mitochondrial FAO (P <0.05). These data show that inhibited mitochondrial FAO in fish induces energy homeostasis remodeling and enhances glucose utilization and protein deposition. Therefore, fish with inhibited mitochondrial FAO could have high potential to utilize carbohydrate. Our results demonstrate a potentially new approach for increasing protein deposition through energy homeostasis regulation in cultured animals.

Nitrate And Nitrite Treatment Modulate Performance And Available Fuel Sources In Zebrafish Muscle And Liver

Treatment with nitrate, but not nitrite, improves exercise performance, in part, by increasing availability of metabolic fuels that require less oxygen for energy production. However, the mechanisms by which these inorganic anions produce performance effects is not well understood. PURPOSE: The purpose of this study is to quantify changes in the metabolic state in zebrafish muscle and liver with nitrate and nitrite treatment during exercise using gene expression and metabolomic methods. METHODS: Liver and muscle were collected from adult zebrafish fish exposed to sodium nitrate (606.9 mg NaNO3/L water), sodium nitrite (19.5 mg NaNO2/L of water), or control water for 21 days (n= 128-130). Tissues were analyzed by quantitative real-time PCR and 1H-NMR untargeted metabolomics. RESULTS: Nitrate treatment significantly increased expression of peroxisome proliferator activated receptor-γ (pparg), a gene involved in regulation of lipid and glucose metabolism. In contrast, acetyl-CoA carboxylase (acaca), a gene that inhibits fatty acid oxidation, significantly decreased in the skeletal muscle of fish treated with nitrate or nitrite as compared to control skeletal muscle tissue. Nitrite treatment also significantly increased carnitine palmitoyl transferase 1b (cpt1b) expression in the liver, which is a primary regulator involved in long-chain fatty acid transport into the mitochondria. Preliminary NMR results show that, relative to control skeletal muscle, nitrate treatment in unexercised fish at rest induces significant increases in metabolic fuels, such as ATP and creatine phosphate, and fuel sources including β-hydroxybutyrate and glycolytic intermediates. After a graded exercise test, the same metabolites increased in control but were decreased in skeletal muscle of nitrate-treated, exercised fish. CONCLUSIONS: Our data are consistent with the hypothesis that nitrate treatment may alter lipid and carbohydrate metabolism of zebrafish, in part, through a PPAR-γ mediated mechanism in the liver, and may improve exercise performance through utilization of fuel sources that require less oxygen during exercise. In contrast, our data indicate that nitrite may increase oxygen cost of exercise, in part, by promoting dependence on fatty acid oxidation in the liver of zebrafish.

Nitrate and Nitrite Treatment Modulate Performance and Available Fuel Sources In Zebrafish Muscle and Liver

Abstract Objectives Treatment with nitrate, but not nitrite, improves exercise performance but the mechanisms responsible are not fully understood. Thus, we tested the hypothesis that nitrate and nitrite treatment alter exercise performance through regulation of genes related to glucose and lipid metabolism in skeletal muscle and liver. Furthermore, we tested the hypothesis that nitrate treatment caused increased abundance and utilization of metabolic fuels in muscle that require less oxygen for energy production. Methods Adult zebrafish fish were exposed to sodium nitrate (606.9 mg NaNO3/L water), sodium nitrite (19.5 mg NaNO2/L of water), or control water for 21 days (n = 9–12/treatment). Liver and muscle gene expression were analyzed by quantitative real-time PCR and liver and muscle metabolomes were assessed by 1H-NMR untargeted metabolomics. Results Nitrite treatment significantly increased carnitine palmitoyl transferase 1b (cpt1b) expression in the liver and significantly decreased acetyl-CoA carboxylase (acaca) expression in skeletal muscle. Nitrate treatment significantly increased expression of peroxisome proliferator activated receptor-γ (pparg) muscle while acaca significantly decreased in skeletal muscle. Nitrate treatment also induced significant increases in metabolic fuels, such as ATP and creatine phosphate, and fuel sources including β-hydroxybutyrate and glycolytic intermediates in rested skeletal muscle. After a graded exercise test, these metabolites decreased in skeletal muscle of nitrate-treated fish while they increased with exercise in the skeletal muscle of control-treated zebrafish. Conclusions Our data are consistent with the hypothesis that nitrate treatment altered lipid and carbohydrate metabolism of zebrafish, in part, through a pparg mediated mechanism in the liver, and may improve exercise performance through utilization of fuel sources that require less oxygen during exercise. In contrast, our data indicate that nitrite may attenuate exercise performance, in part, by promoting dependence on fatty acid oxidation in the liver of zebrafish. These mechanisms may mediate improved exercise tolerance in populations with cardiovascular disease. Funding Sources Celia Strickland and G. Kenneth Austin III Endowment and National Institutes of Health.

αM-Conotoxin MIIIJ Blocks Nicotinic Acetylcholine Receptors at Neuromuscular Junctions of Frog and Fish.

We report the discovery and functional characterization of αM-Conotoxin MIIIJ, a peptide from the venom of the fish-hunting cone snail Conus magus. Injections of αM-MIIIJ induced paralysis in goldfish (Carassius auratus) but not mice. Intracellular recording from skeletal muscles of fish (C. auratus) and frog (Xenopus laevis) revealed that αM-MIIIJ inhibited postsynaptic nicotinic acetylcholine receptors (nAChRs) with an IC50 of ~0.1 μM. With comparable potency, αM-MIIIJ reversibly blocked ACh-gated currents (IACh) of voltage-clamped X. laevis oocytes exogenously expressing nAChRs cloned from zebrafish (Danio rerio) muscle. αM-MIIIJ also protected against slowly-reversible block of IACh by α-bungarotoxin (α-BgTX, a snake neurotoxin) and α-conotoxin EI (α-EI, from Conus ermineus another fish hunter) that competitively block nAChRs at the ACh binding site. Furthermore, assessment by fluorescence microscopy showed that αM-MIIIJ inhibited the binding of fluorescently-tagged α-BgTX at neuromuscular junctions of X. laevis, C. auratus, and D. rerio. (Note, we observed that αM-MIIIJ can block adult mouse and human muscle nAChRs exogenously expressed in X. laevis oocytes, but with IC50s ~100-times higher than those of zebrafish nAChRs.) Taken together, these results indicate that αM-MIIIJ inhibits muscle nAChRs and furthermore apparently does so by interfering with the binding of ACh to its receptor. Comparative alignments with homologous sequences identified in other fish hunters revealed that αM-MIIIJ defines a new class of muscle nAChR inhibitors from cone snails.

Influence of aquatic colloids on the bioaccumulation and biological effects of diclofenac in zebrafish (Danio rerio)

Natural aquatic colloids play an important role in the migration, transformation of pollutants in the environment, but their potential effects are often ignored in ecotoxicology research. In this study, diclofenac (DCF) was selected as a typical drug to study the effects of natural colloids on the bioaccumulation and biotoxicity in juvenile zebrafish (Danio rerio) exposed to an environmentally relevant concentration (1μg/L) and a high concentration (100μg/L) of DCF. The results showed that the presence of colloids accelerated and enhanced the accumulation of DCF in zebrafish muscle and viscera, and the effects are greater at the environmentally relevant concentration of DCF. However, the colloids enhanced the burden in the head in the environmentally relevant concentration group, but reduced it in the high concentration group. This observation may be related to the occurrence of variations in the contribution of the adsorption forms of DCF and the colloids depending on different DCF concentrations. At the same time, the presence of colloids can significantly induce AChE activity of DCF in the brain and alter swimming activity and shoaling behaviour of the individuals, however no significant effects on the attack and shock behaviour were observed. These findings indicate that the combination of natural colloids and pollutants may change with pollutant concentrations, thereby altering the bioaccumulation and biological effects in aquatic organisms.

Intracellular Localization in Zebrafish Muscle and Conserved Sequence Features Suggest Roles for Gelatinase A Moonlighting in Sarcomere Maintenance.

Gelatinase A (Mmp2 in zebrafish) is a well-characterized effector of extracellular matrix remodeling, extracellular signaling, and along with other matrix metalloproteinases (MMPs) and extracellular proteases, it plays important roles in the establishment and maintenance of tissue architecture. Gelatinase A is also found moonlighting inside mammalian striated muscle cells, where it has been implicated in the pathology of ischemia-reperfusion injury. Gelatinase A has no known physiological function in muscle cells, and its localization within mammalian cells appears to be due to inefficient recognition of its N-terminal secretory signal. Here we show that Mmp2 is abundant within the skeletal muscle cells of zebrafish, where it localizes to the M-line of sarcomeres and degrades muscle myosin. The N-terminal secretory signal of zebrafish Mmp2 is also challenging to identify, and this is a conserved characteristic of gelatinase A orthologues, suggesting a selective pressure acting to prevent the efficient secretion of this protease. Furthermore, there are several strongly conserved phosphorylation sites within the catalytic domain of gelatinase A orthologues, some of which are phosphorylated in vivo, and which are known to regulate the activity of this protease. We conclude that gelatinase A likely participates in uncharacterized physiological functions within the striated muscle, possibly in the maintenance of sarcomere proteostasis, that are likely regulated by kinases and phosphatases present in the sarcomere.

Unraveling the pathophysiology of Bethlem Myopathy using a unique zebrafish model for the disease

Bethlem myopathy (BM) is a neuromuscular disease characterized by joint contractures and muscle weakness. BM is caused by mutations in one of the genes encoding one of the three α-chains of collagen VI (COLVI), a component of the skeletal muscle extracellular matrix. Nowadays, an unresolved question is to understand how alteration of COLVI located outside the muscle cells leads to functional modifications in muscle fibers. The zebrafish model col6a1Δex14 is currently the unique animal model of the disease since it is the only model to reproduce a mutation that is the most frequently found in BM patients. In patient and col6a1Δex14 zebrafish muscles, the structure of the sarcoplasmic reticulum has been found to be altered, thus suggesting dysfunction in intracellular Ca2+ handling and/or in ion channels that are known to control Ca2+ homeostasis and to play pivotal roles in muscle function and pathogenesis. Therefore, our project aims at exploring the properties of ion channels and intracellular Ca2+ regulation using electrophysiological approaches and intracellular Ca2+ measurement at rest and during activity in isolated muscle fibers from col6a1Δex14 zebrafish. On one hand, this project should contribute to decipher how alteration in an extracellular matrix component transduces pathogenic signals within muscle fiber and should possibly lead to identify therapeutic targets for this currently incurable disease. On the other hand, because functional studies on zebrafish muscle cells are scarce, this project will provide a sound database on the electrophysiological properties of this cell model.

Myomesin is part of an integrity pathway that responds to sarcomere damage and disease.

The structure and function of the sarcomere of striated muscle is well studied but the steps of sarcomere assembly and maintenance remain under-characterized. With the aid of chaperones and factors of the protein quality control system, muscle proteins can be folded and assembled into the contractile apparatus of the sarcomere. When sarcomere assembly is incomplete or the sarcomere becomes damaged, suites of chaperones and maintenance factors respond to repair the sarcomere. Here we show evidence of the importance of the M-line proteins, specifically myomesin, in the monitoring of sarcomere assembly and integrity in previously characterized zebrafish muscle mutants. We show that myomesin is one of the last proteins to be incorporated into the assembling sarcomere, and that in skeletal muscle, its incorporation requires connections with both titin and myosin. In diseased zebrafish sarcomeres, myomesin1a shows an early increase of gene expression, hours before chaperones respond to damaged muscle. We found that myomesin expression is also more specific to sarcomere damage than muscle creatine kinase, and our results and others support the use of myomesin assays as an early, specific, method of detecting muscle damage.

Streptomycin Pharmaceutical Wastewater affects the T-AOC and CAT activity of Zebrafish

Streptomycin is increasingly being used to treat human diseases. Recently, its toxic effects on aquatic organisms have attracted global attention. The aim of this study was to investigate the toxic effects of streptomycin on zebrafish by measuring T-AOC and CAT activity. Zebrafish were exposed to four different volume concentrations of streptomycin wastewater and their T-AOC and CAT activities were measured at 3, 6, 9, 12 and 15 days. T-AOC activity shows an inverted “N” trend, and T-AOC activity reached the maximum (1.90U·mgprot−1) on the 12th days. Furthermore, The CAT activity shows “M” tendency, and concentrations of streptomycin can affect CAT activity. Streptomycin wastewater induced oxidative stress in Zebrafish muscle tissue.

Single cell dynamics of embryonic muscle progenitor cells in zebrafish.

Muscle stem cells hold a great therapeutic potential in regenerating damaged muscles. However, the in vivo behavior of muscle stem cells during muscle growth and regeneration is still poorly understood. Using zebrafish as a model, we describe the in vivo dynamics and function of embryonic muscle progenitor cells (MPCs) in the dermomyotome. These cells are located in a superficial layer external to muscle fibers and express many extracellular matrix (ECM) genes, including collagen type 1 α2 (col1a2). Utilizing a new col1a2 transgenic line, we show that col1a2+ MPCs display a ramified morphology with dynamic cellular processes. Cell lineage tracing demonstrates that col1a2+ MPCs contribute to new myofibers in normal muscle growth and also during muscle regeneration. A combination of live imaging and single cell clonal analysis reveals a highly choreographed process of muscle regeneration. Activated col1a2+ MPCs change from the quiescent ramified morphology to a polarized and elongated morphology, generating daughter cells that fuse with existing myofibers. Partial depletion of col1a2+ MPCs severely compromises muscle regeneration. Our work provides a dynamic view of embryonic muscle progenitor cells during zebrafish muscle growth and regeneration.

Effect of Ampicillin wastewater on the T-AOC and LDH activities of Zebrafish

In order to define eco-toxicity effect of Ampicillin wastewater on zebrafish, the indoor exposure method was used to study the impact of Ampicillin wastewater on zebrafish. In this study, zebrafish was exposed to ampicillin wastewater of 0.5%, 1.0%, 1.5% and 2.0% groups for 15 days to study the effect of T-AOC (Total Antioxidative Capacity) and LDH (Lactate Dehydrogenase) activities. According to the experimental data, the T-AOC and LDH activities in zebrafish muscle tissue had changed significantly during the period of exposure. The experimental results showed that the T-AOC value of zebrafish in each exposed group showed a “Λ” type change trend. On the 6th day, the 2.0% exposed group reached the maximum value of the whole test period (6.5399U•mg−1). The change of LDH activity was similar to that of T-AOC activity, showing a trend of “sharp increase--decline”. Among them, on the 12th day, the 1% exposed group reached the maximum (792.28 U•mg−1). The research shows ampicillin wastewater can cause some degree of oxidative damage to zebrafish.

Iron and manganese present in underground water promote biochemical, genotoxic, and behavioral alterations in zebrafish (Danio rerio).

Iron (Fe) and manganese (Mn) are metals commonly found at high concentrations in underground water. These metals are essential for the good functioning of living organisms, but high concentrations lead to imbalance, potentiating the appearance of pathologies. This study aimed to evaluate the effect of exposure to naturally occurring metals in groundwater, using zebrafish (Danio rerio) as an experimental model. Thus, zebrafish were exposed to Fe (0.8 and 1.3mg/L), Mn (0.2 and 0.4mg/L), and groundwater collected from deep tube wells with Fe and Mn (Fe 0.8/Mn 0.2mg/L and Fe 1.3/Mn 0.4mg/L) for 30days. Bioaccumulation of these metals has been demonstrated in the livers and muscles of zebrafish. Acetylcholinesterase activity changed only in zebrafish muscles in all groups. Sulfhydryl levels changed mainly in the group Mn 0.4. SOD/CAT ratio decreased in the groups Fe 0.8 and 1.3, Mn 0.4, and Fe 0.8/Mn 0.4. An increase in the frequency of micronucleus in all groups was shown as a consequence of these changes. Behavioral parameters (time and distance traveled, mean speed, turn angle, latency, and number of crossings between compartments) have also changed, mainly in the groups Fe 1.3, Mn 0.4, and Fe 1.3/Mn 0.4. Therefore, long-term exposure to Fe and Mn, even at not so high concentrations, may cause biochemical, genotoxic, and behavioral changes in zebrafish.

The Popeye domain containing gene family encoding a family of cAMP-effector proteins with important functions in striated muscle and beyond

The Popeye domain containing (POPDC) gene family encodes a novel class of membrane-bound cyclic AMP effector proteins. POPDC proteins are abundantly expressed in cardiac and skeletal muscle. Consistent with its predominant expression in striated muscle, Popdc1 and Popdc2 null mutants in mouse and zebrafish develop cardiac arrhythmia and muscular dystrophy. Likewise, mutations in POPDC genes in patients have been associated with cardiac arrhythmia and muscular dystrophy phenotypes. A membrane trafficking function has been identified in this context. POPDC proteins have also been linked to tumour formation. Here, POPDC1 plays a role as a tumour suppressor by limiting c-Myc and WNT signalling. Currently, a common functional link between POPDC’s role in striated muscle and as a tumour suppressor is lacking. We also discuss several alternative working models to better understand POPDC protein function.

Effects of hyperthyroidism in the development of the appendicular skeleton and muscles of zebrafish, with notes on evolutionary developmental pathology (Evo-Devo-Path)

The hypothalamus-pituitary-thyroid (HPT) axis plays a crucial role in the metabolism, homeostasis, somatic growth and development of teleostean fishes. Thyroid hormones regulate essential biological functions such as growth and development, regulation of stress, energy expenditure, tissue compound, and psychological processes. Teleost thyroid follicles produce the same thyroid hormones as in other vertebrates: thyroxin (T4) and triiodothyronine (T3), making the zebrafish a very useful model to study hypo- and hyperthyroidism in other vertebrate taxa, including humans. Here we investigate morphological changes in T3 hyperthyroid cases in the zebrafish to better understand malformations provoked by alterations of T3 levels. In particular, we describe musculoskeletal abnormalities during the development of the zebrafish appendicular skeleton and muscles, compare our observations with those recently done by us on the normal developmental of the zebrafish, and discuss these comparisons within the context of evolutionary developmental pathology (Evo-Devo-Path), including human pathologies.

The neurotoxicity assessment in addicted adult zebrafish (DANIO RERIO) induced by mitragyna speciosa

Kratom (Mitragyna speciosa) belongs to Rubiaceae family. The widely usage for kratom by population in Southeast Asia can leads to dependence with unknown effect on behavioral changes by acute and chronic administration. The aim of this study was to investigate kratom effects towards zebrafish by exploring its potential to alter pathological effects towards the brain and skeletal muscle in adult zebrafish. The adult zebrafish (n=5) were exposed to three different concentrations (50, 150, 250 mg/L). Each adult zebrafish was analyzed through behavior study by CPP test after 4 weeks of treatment. The brain and skeletal muscle morphology changes was observed histologically. Histologically, shown granular cells increase in brain and swelling of skeletal muscle fibers compared to control. These data suggest that the short term and long term exposure of kratom consumption significantly cause degenerative loss of muscle and granular cells increasing.

斑马鱼肌肉结构的定量偏振成像

斑马鱼肌肉结构的定量偏振成像

Acute hypoxia/reoxygenation affects muscle mitochondrial respiration and redox state as well as swimming endurance in zebrafish.

Rapid fluctuations of the oxygen content of both natural and anthropogenic origin are relatively common in freshwater environments. Fish adaptation to these conditions implies tolerance of both low levels of oxygen availability and reoxygenation. Hypoxia tolerance in fish has been widely studied, but the involvement of mitochondria in the response of fish to rapid hypoxia/reoxygenation stress is less known. Zebrafish, a floodplain species, is likely facing significant changes in dissolved oxygen in its natural environment and displays a moderate ability to tolerate hypoxia. In the present study, we report the effects of an acute hypoxia/reoxygenation stress (H/R) protocol on mitochondrial functionality (respiration, complex activities, rate of H2O2 release) and redox state (level of HPs and protein oxidation) of muscle tissue. In parallel, the animal metabolic performance (routine metabolism, nitrogen excretion and swimming performance) was measured. Additionally, the recovery from H/R was tested 20h after treatment. A significant stimulation by H/R of muscle mitochondrial respiration and H2O2 release was observed, which was only in part counteracted by stimulation of the antioxidant system, resulting in an increased level of lipid peroxides and protein carbonyls. In parallel, H/R increased the animal oxygen consumption and urea excretion rate and reduced routine activity. A significant strong reduction of endurance at 80% Ucrit was also observed. Most of the altered parameter did not recover 20h after reoxygenation. These data indicate a significant alteration of zebrafish muscle mitochondrial state after acute H/R, associated with changes in tissue redox state and locomotor performance.

Toxicity responses of different organs of zebrafish (Danio rerio) to silver nanoparticles with different particle sizes and surface coatings

Silver nanoparticles (AgNPs) in aquatic ecosystems are toxic to aquatic organisms. In this study, we aimed to investigate the toxicities and molecular mechanisms of AgNPs with different surface coatings (sodium citrate and polyvinylpyrrolidone) and particle sizes (20 nm and 100 nm) in the gills, intestines, and muscles of zebrafish after 96 h of exposure. Our results indicated that the contribution of particle size to AgNP toxicity was greater than that of the surface coating. Citrate-coated AgNPs were more toxic than polyvinylpyrrolidone-coated AgNPs, and 20-nm AgNPs were more toxic than 100-nm AgNPs. The toxic effects of AgNPs to the tissues were in the order intestines > gills > muscles. Differential expression of genes with the different AgNPs confirmed that they had toxic effects in the zebrafish tissues at the molecular level. Our comprehensive comparison of the toxicities of different AgNPs to aquatic ecosystems will be helpful for further risk assessments of AgNPs.

Generation and characterization of a zebrafish muscle specific inducible Cre line.

Zebrafish transgenic lines provide valuable insights into gene functions, cell lineages and cell behaviors during development. Spatiotemporal control over transgene expression is a critical need in many experimental approaches, with applications in loss- and gain-of-function expression, ectopic expression and lineage tracing experiments. The Cre/loxP recombination system is a powerful tool to provide this control and the demand for validated Cre and loxP zebrafish transgenics is high. One of the major challenges to widespread application of Cre/loxP technology in zebrafish is comparatively small numbers of established tissue-specific Cre or CreERT2 lines. We used Tol2-mediated transgenesis to generate Tg(CrymCherry;-1.9mylz2:CreERT2) which provides an inducible CreERT2 source driven by muscle-specific mylz2 promoter. The transgenic specifically labels the trunk and tail skeletal muscles. We assessed the temporal responsiveness of the transgenic by screening with a validated loxP reporter transgenic ubi:Switch. Further, we evaluated the recombination efficiency in the transgenic with varying concentrations of 4-OHT, for different induction time periods and at different stages of embryogenesis and observed that higher recombination efficiency is achieved when embryos are induced with 10μM 4-OHT from 10-somites or 24 hpf till 48 or 72 hpf. The transgenic is an addition to currently available zebrafish transgenesis toolbox and a significant tool to advance muscle biology studies in zebrafish.