Muscle Formation Research Articles

3D-environment and muscle contraction regulate the heterogeneity of myonuclei.

Skeletal muscle formation involves tight interactions between muscle cells and associated connective tissue fibroblasts. Every muscle displays the same type of organisation, they are innervated in the middle and attached at both extremities to tendons. Myonuclei are heterogeneous along myotubes and regionalised according to these middle and tip domains. During development, as soon as myotubes are formed, myonuclei at muscle tips facing developing tendons display their own molecular program. In addition to molecular heterogeneity, a subset of tip myonuclei has a fibroblastic origin different to the classical somitic origin, highlighting a cellular heterogeneity of myonuclei in foetal myotubes. To gain insights on the functional relevance of myonucleus heterogeneity during limb development, we used 2D culture and co-culture systems to dissociate autonomous processes (occurring in 2D-cultures) from 3D-environment of tissue development. We also assessed the role of muscle contraction in myonucleus heterogeneity in paralysed limb muscles. The regionalisation of cellular heterogeneity was not observed in 2D cell culture systems and paralyzed muscles. The molecular signature of MTJ myonuclei was lost in a dish and paralysed muscles indicating a requirement of 3D-enviroment and muscle contraction for MTJ formation. Tip genes that maintain a regionalized expression at myotube tips in cultures are linked to sarcomeres. The behaviour of regionalized markers in cultured myotubes and paralyzed muscles allows us to speculate whether the genes intervene in myogenesis, myotube attachment or MTJ formation.

SMN depletion impairs skeletal muscle formation and maturation in a mouse model of SMA.

Spinal muscular atrophy (SMA) is characterized by low levels of the ubiquitously expressed Survival Motor Neuron (SMN) protein, leading to progressive muscle weakness and atrophy. Skeletal muscle satellite cells play a crucial role in muscle fiber maintenance, repair, and remodelling. While the effects of SMN depletion in muscle are well documented, its precise role in satellite cell function remains largely unclear. Using the Smn2B/- mouse model, we investigated SMN-depleted satellite cell biology through single fiber culture studies. Myofibers from Smn2B/- mice were smaller in size, shorter in length, had reduced myonuclear domain size, and reduced sub-synaptic myonuclear clusters-all suggesting impaired muscle function and integrity. These changes were accompanied by a reduction in the number of myonuclei in myofibers from Smn2B/- mice across all disease stages examined. Although the number of satellite cells in myofibers was significantly reduced, those remaining retained their capacity for myogenic activation and proliferation. These findings support the idea that a dysregulated myogenic process could be occurring as early in muscle stem cells during muscle formation and maturation in SMA. Targeting those pathways could offer additional options for combinatorial therapies for SMA.

Selection of farm guinea fowls for compatibility

As a result of many years of work by us, in the peasant farm K.A. Zhdanov (Voronezh region, Ramonsky district, Novopodkletnoye village) on the basis of guinea fowl of the Volga white breed, the paternal (VBA-1) and maternal (VB-4) lines of guinea fowl were preserved and evaluated. The yield of guinea fowl from one hen over 64 weeks of life is 74–77 heads. Anatomical cutting of poultry and calculation of body indexes of females and males of the VBA-1 and VB-4 lines and interline hybrids showed the superiority of the latter over the parent forms, in terms of the massiveness index by 2.89–6.9%, keel development and high-legged index by 0. 58-0.35%. According to the broad-body index, birds of the VBA-1 and VBA-2 lines were superior to hybrid guinea fowl by 0.2–2.22%. In terms of keel development, hybrids of the VBA-12 line exceeded the parent lines by 0.98–5.0%, which indicates their greater compactness, massiveness and muscularity (formation of the pectoral muscles in width). The results of anatomical cutting of carcasses indicate higher meat qualities of hybrid poultry, since the yield of edible parts of hybrids was 0.04% higher.

Effect of NR1D1 on the proliferation and differentiation of yak skeletal muscle satellite cells

The severe conditions at high altitudes, where yaks inhabit, contribute to delayed muscular growth and compromised tenderness of their muscle tissue. Myosatellite cells are responsible for the growth and regeneration of skeletal muscle after birth and have the potential to proliferate and differentiate, its development is closely related to meat quality, and the nuclear receptor gene NR1D1 is involved in muscle formation and skeletal muscle regulation. Therefore, in order to understand the effect of NR1D1 on muscle satellite cells, we identified the mRNA expression levels of marker genes specifically expressed in muscle satellite cells at different stages to determine the type of cells isolated. Eventually, we successfully constructed a primary cell line of yak muscle satellite cells. Then we constructed NR1D1 overexpression vector and interference RNA, and introduced them into isolated yak skeletal muscle satellite cells. We performed qPCR, CCK8, and fluorescence-specific to detect the expression of genes or abundance of proteins as markers of cell proliferation and differentiation. Compared with those in the control group, the expression levels of proliferation marker genes KI-67, CYCLIND1, and CYCLINA were significantly inhibited after NR1D1 overexpression, which was also supported by the CCK-8 test, whereas differentiation marker genes MYOD, MYOG, and MYF5 were significantly inhibited. Fluorescence-specific staining showed that KI-67 protein abundance and the number of microfilaments both decreased, while the opposite trend was observed after NR1D1 interference. In conclusion, we confirmed that NR1D1 inhibited the proliferation and differentiation of yak skeletal muscle satellite cells, which provides a theoretical basis for further research on the effect of NR1D1 on improving meat quality traits and meat production performance of yaks.

Fibrodysplasia ossificans progressiva: a comprehensive review

Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder that causes heterotopic ossification of soft tissues, leading to abnormal bone growth in muscles, tendons, and ligaments. First identified in the 17th century, FOP was classified in 1968 and is linked to a mutation in the Activin A receptor type I gene (ACVR1) which affects bone morphogenetic protein (BMP). The autosomal dominant condition FOP has the potential to lead to aberrant bone development. At birth, FOP individuals appear normal, except for characteristic malformations of the great toes. FOP patients develop painful, inflammatory soft tissue swellings during the first decade of life, often precipitated by soft tissue injury. Minor trauma can trigger new flare-ups and leads to progressive heterotopic ossification. Most FOP sufferers are wheelchair-bound by their third decade and needs lifelong assistance with daily living tasks. Bone morphogenetic proteins (BMPs) are bound by the transmembrane kinase receptor ALK2, which is encoded by the (ACVR1/ALK2 gene). FOPs induce heterotopic bone formation in skeletal muscle and can be caused by mutations in the activin A receptor type I (ACVR1) and activin-like kinase 2 (ALK2) gene. Clinical therapy focuses on preventing and controlling inflammation, with ongoing research focusing on specific therapies targeting receptor activity, aberrant pathways, or cellular components influencing bone neo-formation.

The T-Type Calcium Channel CACNA1H is Required for Smooth Muscle Cytoskeletal Organization During Tracheal Tubulogenesis.

Abnormalities of tracheal smooth muscle (SM) formation are associated with several clinical disorders including tracheal stenosis and tracheomalacia. However, the cellular and molecular mechanisms underlying tracheal SM formation remain poorly understood. Here, it is shown that the T-type calcium channel CACNA1H is a novel regulator of tracheal SM formation and contraction. Cacna1h in an ethylnitrosourea forward genetic screen for regulators of respiratory disease using the mouse as a model is identified. Cacna1h mutants exhibit tracheal stenosis, disorganized SM and compromised tracheal contraction. CACNA1H is essential to maintain actin polymerization, which is required for tracheal SM organization and tube formation. This process appears to be partially mediated through activation of the actin regulator RhoA, as pharmacological increase of RhoA activity ameliorates the Cacna1h-mutant trachea phenotypes. Analysis of human tracheal tissues indicates that a decrease in CACNA1H protein levels is associated with congenital tracheostenosis. These results provide insight into the role for the T-type calcium channel in cytoskeletal organization and SM formation during tracheal tube formation and suggest novel targets for congenital tracheostenosis intervention.

Integrated Analysis Reveals Genetic Basis of Growth Curve Parameters in an F2 Designed Pig Population Based on Genome and Transcriptome Data

Appropriate growth curves can reflect more sophisticated growth patterns of animals than body weight, and thus, the identification of genes and variants related to the growth curve parameter traits contributes to revealing the fine growth and development characteristics of livestock. However, the ability of single genome-wide association analysis (GWAS) and transcriptome analyses to identify valuable genes and variants is limited. In this study, based on genome and transcriptome data, the growth curve parameter traits of hybrid pigs were analyzed, and a set of genes and variants were identified. The Gompertz–Laird growth curve model was optimized to reveal the growth pattern of F2 individuals of Duroc × Erhualian pigs over four time points. Five growth parameters were estimated, including initial body weight (W0), instantaneous growth rate per day (L), coefficient of relative growth or maturing index (k), body weight at inflection point (Wi), and average growth rate (GR). These five parameters were subjected to a genome-wide association study, differential gene expression analysis, and weighted gene co-expression network analysis (WGCNA). In the study, 336 pigs were genotyped, and 39,494 SNP markers were used for each pig in the analysis. Thirty of these pigs were also included in the transcriptomics analysis. Based on genome and transcriptome data, the integrated analyses identified five putative SNPs (including INRA0056460 on chromosome X, DRGA0004151 on chromosome 3, INRA0056460 on chromosome X, H3GA0049324 on chromosome 17, and H3GA0037747 on chromosome 13) and 15 candidate genes (PDGFA, VEGFD, CSPP1, EFHC1, PIK3C3, ZZZ3, GCC2, MAPK14, ZPR1, ISG15, ANG, CEBPD, ZHX3, CTBP2, and MYNN). The functional analysis indicated that these candidate genes played important roles in cell division and differentiation, development and aging, and skeletal muscle and fat formation. Our results provide insight into the genetic mechanisms underlying the growth and development of hybrid pigs and offer a theoretical basis for genomic breeding.

Tubular Aggregates as a Marker of Aging in Skeletal Muscle.

Tubular aggregates (TA) are skeletal muscle structures that arise from the progressive accumulation of sarcoplasmic reticulum proteins, mainly with aging. Muscle regeneration plays a role in TA formation. TA quantification may aid in the evaluation of muscle aging and genetic muscle degeneration. TA form over time, appears in aging in normal murine muscles. TA reduction in injured conditions may be due to the degeneration-regeneration process in muscles, with loss of damaged muscle fibers and formation of new fibers that do not present protein aggregation. These new regenerated fibers do not improve the function capacity of the aged muscle. Here, we present a methodology for labeling and identifying tubular aggregates in muscle fibers and also the standardization of its quantification.

PEMBUATAN PUDING BERBAHAN DASAR DAUN KELOR SEBAGAI UPAYA PENCEGAHAN STUNTING DI DESA SINDANGMULYA

Malnutrition in children can cause delays in growth and development of the brain, bones, and emotional problems. This service program aims to provide understanding to the community, especially prospective parents, about stunting and the benefits of moringa Puding. Moringa leaf Puding has important benefits in preventing stunting, especially because of the very complete nutritional content of moringa leaves. Moringa leaves are rich in protein, vitamins A, C, E, calcium, and iron, all of which play an important role in supporting children's growth and development. The protein and calcium in moringa help in the formation of healthy bones and muscles, while iron plays a role in preventing anemia that can hinder growth. Vitamins A and C support the immune system, which is important for keeping children healthy and preventing infections that can hinder growth. The activity was conducted in two stages, starting with providing information on stunting and child nutrition. The next stage involved a demonstration of making moringa Puding. The results of this program were adequate knowledge about the types of nutritional intake that are good for children as a prevention of stunting and the community was able to make nutritious Puding made from moringa leaves.

Coil Formation and Biomimetic Performance Characterization of Twisted Coiled Polymer Artificial Muscles

A biological muscle's force is nonlinearly constrained by its current state (force, length, and speed) and state history. To investigate if artificial muscles can mimic (i.e. biomimetic) the complete mechanical state spectrum of biological muscles, this study uses a novel method to characterize twisted coiled polymer actuators (TCPAs) mechanically. Thus, comprehensive and reproducible test procedures are established to verify artificial muscle biomimetics regarding stress, strain, and strain rate combinations intrinsic to biological muscle. A rheometer performs novel high‐precision mechanical characterization methods to comprehensively verify biomimetic performance. Sample twist level, torque, length, force, and temperature are controlled and measured during twist‐induced coiling, heatsetting/annealing, and mechanical testing. TCPAs are formed from linear low‐density polyethylene monofilament. Linear low‐density polyethylene (LLDPE) TCPAs generate larger stresses than biological muscle through the entire spectrum of strains—contracting more than 40%, exerting more than 0.3 MPa at rest length, and withstanding tension of 8 MPa without damage. Thus, the LLDPE TCPAs attain biological muscle performance statically, but additional tests are required to assess this dynamically. The mechanical performance of LLDPE TCPAs enables biomimetic actuation with an intelligent control and measurement system. Their high‐throughput textile manufacturability positions them for advanced biomechatronic applications—including prosthetics and exoskeletons.

Impacts of Intermittent Fasting on Floc Formation, Growth, Chemical Composition, and Histomorphometry of Muscles of the Nile Tilapia Cultured in the Biofloc System

Impacts of Intermittent Fasting on Floc Formation, Growth, Chemical Composition, and Histomorphometry of Muscles of the Nile Tilapia Cultured in the Biofloc System

Spatial Transcriptomics Analysis: Maternal Obesity Impairs Myogenic Cell Migration and Differentiation during Embryonic Limb Development.

Limb muscle is responsible for physical activities and myogenic cell migration during embryogenesis is indispensable for limb muscle formation. Maternal obesity (MO) impairs prenatal skeletal muscle development, but the effects of MO on myogenic cell migration remain to be examined. C57BL/6 mice embryos were collected at E13.5. The GeoMx DSP platform was used to customize five regions along myogenic cell migration routes (myotome, dorsal/ventral limb, limb stroma, limb tip), and data were analyzed by GeomxTools 3.6.0. A total of 2224 genes were down-regulated in the MO group. The GO enrichment analysis showed that MO inhibited migration-related biological processes. The signaling pathways guiding myogenic migration such as hepatocyte growth factor signaling, fibroblast growth factor signaling, Wnt signaling and GTPase signaling were down-regulated in the MO E13.5 limb tip. Correspondingly, the expression levels of genes involved in myogenic cell migration, such as Pax3, Gab1, Pxn, Tln2 and Arpc, were decreased in the MO group, especially in the dorsal and ventral sides of the limb. Additionally, myogenic differentiation-related genes were down-regulated in the MO limb. MO impedes myogenic cell migration and differentiation in the embryonic limb, providing an explanation for the impairment of fetal muscle development and offspring muscle function due to MO.

Moesin controls cell-cell fusion and osteoclast function.

Cell-cell fusion is an evolutionarily conserved process that is essential for many functions, including fertilisation and the formation of placenta, muscle and osteoclasts, multinucleated cells that are unique in their ability to resorb bone. The mechanisms of osteoclast multinucleation involve dynamic interactions between the actin cytoskeleton and the plasma membrane that are still poorly characterized. Here, we found that moesin, a cytoskeletal linker protein member of the Ezrin/Radixin/Moesin (ERM) protein family, is activated during osteoclast maturation and plays an instrumental role in both osteoclast fusion and function. In mouse and human osteoclast precursors, moesin inhibition favors their ability to fuse into multinucleated osteoclasts. Accordingly, we demonstrated that moesin depletion decreases membrane-to-cortex attachment and enhances the formation of tunneling nanotubes (TNTs), F-actin-based intercellular bridges that we reveal here to trigger cell-cell fusion. Moesin also controls HIV-1- and inflammation-induced cell fusion. In addition, moesin regulates the formation of the sealing zone, the adhesive structure determining osteoclast bone resorption area, and thus controls bone degradation, via a β3-integrin/RhoA/SLK pathway. Supporting our results, moesin - deficient mice present a reduced density of trabecular bones and increased osteoclast abundance and activity. These findings provide a better understanding of the regulation of cell-cell fusion and osteoclast biology, opening new opportunities to specifically target osteoclast activity in bone disease therapy.

A myogenic regulatory factor is required for myogenesis during limb regeneration in the Chinese mitten crab

Myogenic regulatory factors (MRFs) are a group of transcription factors that regulate the activity of skeletal muscle cells during embryonic development and postnatal myogenesis in various vertebrate species. However, the role of MRFs in limb regeneration remains poorly understood in crustaceans. In this study, we identified a full-length cDNA encoding a myogenic regulatory factor from Eriocheir sinensis (EsMRF) and evaluated its mRNA expression profile during muscle development, growth, and regeneration. The expression of EsMRF was found to correlate with the onset of muscle formation during development and with the regeneration process following limb autotomy. To elucidate the function of MRF during limb regeneration in E. sinensis, we assessed regenerative efficiency using RNA interference (RNAi) targeting EsMRF. Our findings revealed that the blockade of MRF delayed limb regeneration by disrupting the proliferation and myogenesis of blastema cells at the basal growth stage. Furthermore, luciferase assays results demonstrated that EsMRF can transcriptionally activate target myogenic genes, either through direct binding to their promoters or by interacting with co-regulators such as EsHEB or EsMEF2. This study identifies a novel MRF in E. sinensis and elucidates its function during limb regeneration, thereby contributing to our understanding of muscle growth and regeneration mechanisms in crustaceans.

Inhibition of myotube formation by platelet-derived growth factor subunit B in QM7 cells.

The primary objective of this study was to investigate the role and regulatory mechanisms of Platelet-derived Growth Factor Subunit B (PDGFB) in muscle differentiation. In this study, a vector for PDGFB was designed and transfected into quail muscle cells to investigate its role and regulatory mechanism during muscle formation. To investigate the inhibitory mechanisms of PDGFB on myogenic differentiation, the mRNA expression levels of various genes and the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2), both known to regulate muscle development and differentiation were compared. PDGFB-overexpressed (OE) cells formed morphologically shorter and thinner myotubes and demonstrated a smaller total myotube area than did the control cells. This result was also confirmed at the molecular level by a reduced amount of myosin heavy chain protein in the PDGFB-OE cells. Therefore, PDGFB inhibits the differentiation of muscle cells. Additionally, the expression of myogenin (MYOG) significantly decreased in the PDGFB-OE cells on days 2 and 4 compared with that in the control cells. The phosphorylation of ERK 1/2, an upstream protein that inhibits MYOG expression, increased in the PDGFB-OE cells on day 4 compared with that in the control cells. The decreased expression of MYOG in the PDGFB-OE cells increased by inhibition ERK 1/2 phosphorylation. PDGFB may suppress myogenesis by reducing MYOG expression through ERK 1/2 phosphorylation. These findings can help understand muscle differentiation and potentially improve poultry meat production.

Glutaminase-1 inhibition alleviates senescence of Wharton's jelly-derived mesenchymal stem cells via senolysis.

Replicative senescence of mesenchymal stem cells (MSCs) caused by repeated cell culture undermines their potential as a cell therapy because of the reduction in their proliferation and therapeutic potential. Glutaminase-1 (GLS1) is reported to be involved in the survival of senescent cells, and inhibition of GLS1 alleviates age-related dysfunction via senescent cell removal. In the present study, we attempted to elucidate the association between MSC senescence and GLS1. We conducted in vitro and in vivo experiments to analyze the effect of GLS1 inhibition on senolysis and the therapeutic effects of MSCs. Inhibition of GLS1 in Wharton's jelly-derived MSCs (WJ-MSCs) reduced the expression of aging-related markers, such as p16, p21, and senescence-associated secretory phenotype genes, by senolysis. Replicative senescence-alleviated WJ-MSCs, which recovered after short-term treatment with bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide 3 (BPTES), showed increased proliferation and therapeutic effects compared to those observed with senescent WJ-MSCs. Moreover, compared to senescent WJ-MSCs, replicative senescence-alleviated WJ-MSCs inhibited apoptosis in serum-starved C2C12 cells, enhanced muscle formation, and hindered apoptosis and fibrosis in mdx mice. These results imply that GLS1 inhibition can ameliorate the therapeutic effects of senescent WJ-MSCs in patients with muscle diseases such as Duchenne muscular dystrophy. In conclusion, GLS1 is a key factor in modulating the senescence mechanism of MSCs, and regulation of GLS1 may enhance the therapeutic effects of senescent MSCs, thereby increasing the success rate of clinical trials involving MSCs.

Genome to phenome Association for Pork Belly Parameters Elucidates Three Regulation Distinctions: Adipogenesis, muscle formation, and their transcription factors

Genome to phenome analysis is necessary in livestock areas because of its various and complex phenotypes. Pork belly is a favorable part of meat worldwide, including East Asia. A previous study has suggested that the three key transcription factors (ZNF444, NFYA and PPARG) affecting pork belly traits include total volume, the volume of total fat and muscle, and component muscles of the corresponding slice. However, other transcription factor genes affecting each slice other than pork belly component traits still needed to be identified. Thus, we aimed to analyze pork belly components at the genome to phenome level for identifying key transcription factor genes and their co-associated networks. The range of node numbers against each component trait via the association weight matrix was from 598 to 3020. Premised on the result, an in silico functional approach was performed. Each co-association network enriched three key transcription factors in adipogenesis and skeletal muscle proliferation, mesoderm development, metabolism, and gene transcription. The three key transcription factors and their related genes may be useful in comprehending their effect of pork belly construction.

Preparation and Performance of a Novel Polyurethane Microporous Film on Polypropylene Medical Mesh Surface

This study aims to develop a medical patch surface material featuring a microporous polyurethane (PU) membrane and to assess the material's properties and biological performance. The goal is to enhance the clinical applicability of pelvic floor repair patch materials. PU films with a microporous surface were prepared using PU prepolymer foaming technology. The films were produced by optimizing the PU prepolymer isocyanate index (R value) and the relative humidity (RH) of the foaming environment. The surface morphology of the PU microporous films was observed by scanning electron microscopy, and the chemical properties of the PU microporous films, including hydrophilicity, were analyzed using infrared spectroscopy, Raman spectroscopy, and water contact angle measurements. In vitro evaluations included testing the effects of PU microporous film extracts on the proliferation of L929 mouse fibroblasts and observing the adhesion and morphology of these fibroblasts. Additionally, the effect of the PU microporous films on RAW264.7 mouse macrophages was studied. Immune response and tissue regeneration were assessed in vivo using Sprague Dawley (SD) rats. The PU films exhibited a well-defined and uniform microporous structure when the R value of PU prepolymer=1.5 and the foaming environment RH=70%. The chemical structure of the PU microporous films was not significantly altered compared to the PU films, with a significantly lower water contact angle ([55.7±1.5]° ) compared to PU films ([69.5±1.7]° ) and polypropylene (PP) ([ 104.3±2.5]°), indicating superior hydrophilicity. The extracts from PU microporous films demonstrated good in vitro biocompatibility, promoting the proliferation of L929 mouse fibroblasts. The surface morphology of the PU microporous films facilitated fibroblast adhesion and spreading. The films also inhibited the secretion of tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β by RAW264.7 macrophages while enhancing IL-10 and IL-4 secretion. Compared to 24 hours, after 72 hours of culture, the expression levels of TNF-α and IL-1β were reduced in both the PU film and PU microporous film groups and were significantly lower than those in the PP film group (P<0.05), with the most notable decreases observed in the PU microporous film group. IL-10 and IL-4 levels increased significantly in the PU microporous film group, surpassing those in the PP film group (P<0.01), with the most pronounced increase in IL-4. The PU microporous film induced mild inflammation with no significant fibrous capsule formation in vivo. After 60 days of implantation, the film partially degraded, showing extensive collagen fiber growth and muscle formation in its central region. The PU microporous film exhibits good hydrophilicity and biocompatibility. Its surface morphology enhances cell adhesion, regulates the function of RAW264.7 macrophages, and promotes tissue repair, offering new insights for the design of pelvic floor repair and reconstruction patch materials.

Identifying candidate genes and biological pathways in muscle development through multi-tissue transcriptome comparisons between male and female geese

Males and females have long shown disparities in body weight and height; yet, the underlying mechanisms influencing growth and development remain unclear. Male and female Zhedong White Geese (ZDW) geese have long been selected for large body size and egg production, respectively. This led to a large difference in body weight between males and females, making them a unique model for studying the effects of sex on growth and development. This study aimed to elucidate these mechanisms by comparing the transcriptomes of muscle and pituitary tissues in male and female ZDW geese to identify the critical genes responsible for the effects of sex on growth performance. Our analysis revealed 1101 differentially expressed genes (DEGs) in leg musculature (507 upregulated, 594 downregulated), 773 DEGs in breast musculature (311 upregulated, 462 downregulated), and 517 DEGs in the pituitary gland (281 upregulated, 236 downregulated) between male and female geese. These DEGs were significantly enriched in gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with endocrine metabolism (e.g., hormonal activities), muscle formation (e.g., sarcomere and myofibril), and bone formation (e.g., bone morphogenesis and cartilage formation). The upregulated genes in males were enriched in KEGG pathways involving nutrient digestion and absorption (vitamin and protein), as well as the secretion of digestive juices (gastric acid and bile). Through protein–protein interaction analyses, we also observed high-density gene networks related to muscle fiber development, calcium ion metabolism, mitochondrial respiratory chain, and bone development. Therefore, our multi-tissue transcriptome analysis provides a deeper understanding of the complex and systematic gender-driven effects on growth and development in geese. IGF1, GHRHR, and NCAPG-LCORL and pathways related to myogenesis might play vital roles in gender differences before hormones exert their effect.

Myogenic Regulator Genes Responsible For Muscle Development in Farm Animals

Farm animals especially poultry species play important roles in meeting the worldwide demand for meat and are genetically improved to increase the efficiency of meat production. Improving muscle growth and development is crucial to meet customers' demands for high-quality meat. Myogenesis, fibrogenesis, and adipogenesis are components of fetal skeletal muscle formation. Myogenesis is controlled by a complex network of intrinsic and extrinsic components, usually divided into two or three stages and regulated by kinase-encoding genes and myogenic regulatory factor genes. The basic family of helix-loop-helix transcription factors, which includes MYF5, MYOD, myogenin, and MRF4, regulates the specification and differentiation of skeletal muscle cells throughout embryogenesis and postnatal myogenesis. With the discovery of the myogenic regulatory factor family, which includes the transcription factors MYF5, MYOD, Myogenin, and MRF4, it has become possible to determine the skeletal muscle lineage and understand the regulation of myogenic differentiation during development. These elements also play a role in determining the muscle satellite cell lineage that develops into the resident stem cell compartment in adult skeletal muscle. Although MYF5, MYOD, Myogenin and MRF4 play minor roles in mature muscle, they once again play an important role in directing satellite cell activity to regenerate skeletal muscle, linking the genetic regulation of development and regeneration myogenesis. An important step towards the goal of increasing meat yield and improving meat quality is the understanding and identification of these genes. This in-depth analysis discusses the function of myogenic regulatory factors in the specification of satellite cells, maturation and regeneration of skeletal muscle.