Brief Summary of Minutes of Annual Meeting

Brief Summary of Minutes of Annual Meeting: Members not attending: Rod Hill-Idaho; Mathew E. Doumit-Idaho; Marcia R. Hathaway-Minnesota; Jane A. Boles-Montana; Michael G. Zeece-Nebraska; Michael Dodson-Washington State; The annual meeting of the NC-1131 technical committee meeting was held at the University of Arizona, Tucson on 7-8 November, 2008 and hosted by Dr. Robert Rhoads, Department of Animal Sciences, University of Arizona. The group was welcomed by Dr. Ronald Allen, head of the Department of Animal Science, and Dr. Colin Kaltenbach, the director of Arizona Agricultural Experimental Station. Dr. Kaltenbach gave an overview of agriculture in Arizona and presented problems and opportunities for Arizona agriculture. Following Dr. Kaltenbach's welcome, the remainder of the first day to 4:00pm was filled by oral station reports summarizing each station's contributions to the objectives of the NC-1131 project. After 4:00 pm, there was a special session---remembering Dr. Darrel Goll. In addition to all attending NC1131 members, many faculty members and colleagues of Dr. Goll at University of Arizona also attended the session. The business meeting was held on the next day, chaired by the Administrative Advisor, Dr. Alan Grant. Dr. Grant proposed to form a committee to write the project renewal proposal, which is composed of Drs. Killefer, Riggs and Kuang. Dr. Killefer will take charge of the writing with the assistance from Drs. Riggs and Kuang. The objectives for the renewal were also revised. The new objectives are: 1) Characterize the signal transduction pathways that regulate skeletal muscle growth and metabolism. (TX, IN, NE, AZ, OH, WI, IL, SD, WY, MN, HI, ID) 2) Characterize the cellular and molecular basis of myogenesis. (IN, MN, IL, MI, AZ, SD, OH, WA, NC, WY, FL, ID, HI) 3) Characterize mechanisms of protein assembly and degradation in skeletal muscle. (WI, NE, IN, IL) Dr.Debora Hamernik, the USDA-CSREES representative also introduced the name changes of USDA-CREES to USDA-National Institute for Food and Agriculture (NIFA), and the funding situation and regulations of USDA. Next year's annual meeting of the NC-1131 committee will be held at the University of Wyoming, Laramie, Wyoming at a date yet to be determined. Dr. Penny Riggs, Texas A&M University, was elected as secretary for the 2008-09 year with the expectation that the 2010 meeting will be held in College Station, Texas. Following the business, station reports resumed to the noon. The meeting adjourned at noon to allow participants time to return home that day.

The Arizona Station reported their progress in satellite cell research. Myogenesis is driven by resident stem cells termed satellite cells (SC) whereas angiogenesis arises from endothelial cells and perivascular cells of pre-existing vascular segments and the collateral vasculature. Without proper revascularization of damaged muscle, myogenic cells do not survive and myogenesis ceases. Communication between myogenic and angiogenic cells seems plausible, especially given the number of growth factors produced by SC. To characterize these interactions, they developed an in vitro co-culture model composed of SC and microvascular fragments (MVF). In this system, isolated MVF suspended in collagen gel are cultured over a rat SC monolayer culture. In the presence of SC, MVF exhibit greater indices of angiogenesis than MVF cultured alone. A positive dose-dependent effect of SC conditioned medium (CM) on MVF growth was observed suggesting that SC secrete soluble-acting growth factor(s). Next, they specifically blocked VEGF action in SC CM and this was sufficient to abolish satellite cell-induced angiogenesis. Finally, hypoxia inducible factor-1alpha (HIF-1±), a transcriptional regulator of VEGF gene expression, was found to be expressed in cultured SC and in putative SC in sections of stretch-injured muscle. This data indicates that satellite cell-derived VEGF and HGF play an important role in satellite cell mediated angiogenic processes. Another progress in Arizona Station is to examine the role of environmental influences on skeletal muscle growth, metabolism and physiology. A large proportion of an animal's mass is comprised of skeletal muscle which can have a profound impact on whole-animal energy metabolism and nutrient homeostasis especially during periods of heat stress. They have initiated a series of studies to understand how environmental factors influence the set points of several metabolic pathways within skeletal muscle. Skeletal muscle (semimembranosus) biopsies were obtained from beef cattle during thermal comfort conditions and again after exposure to heat stress conditions. Total RNA was isolated for DNA microarray (GeneChip® Bovine Genome Arrays, Affymetrix, Inc.). Data demonstrated the differential expression of 251 genes based on an adjusted p value of less than 0.005. Interrogation of the data by pathway analysis has revealed dramatic changes in the skeletal muscle transcriptional profile relating to mitochondrial function. It appears that during heat stress bovine skeletal muscle may experience mitochondrial dysfunction leading to impaired cellular energy status. Arizona station also updated their research in calpain system. The calpain system is generally accepted as being responsible for postmortem tenderization of meat. It has been suggested that µ-calpain is responsible for the proteolytic degradation that occurs, however, most of the µ-calpain activity is gone after 3 d of postmortem storage. On the other hand, m-calpain activity can be detected even 14 d postmortem. Both calpastatin and µ-calpain are extensively degraded after 14 d of postmortem storage. In order to better characterize the extent of degradation of these 3 proteins, they have attempted to purify calpains from 12-14 d postmortem bovine semimembranosus. They have identified 5 fractions: 2 fractions of calpastatin activity, CAST I and CAST II, 2 fractions of µ-calpain, and 1 fraction of m-calpain. Purification of m-calpain in postmortem muscle yielded a single fraction with intact 80-kDa and 28-kDa subunits with purity similar to that of at-death purified m-calpain. The specific activity was slightly less (~ 25% lower) than at-death purified m-calpain and total m-calpain protein recovered was much less than for at-death m-calpain. The calcium concentration required for half-maximal activity was the same for both at-death and postmortem m-calpain. The Hawaii station analyzed global gene expression in hypertrophic skeletal muscles induced by clenbuterol and myostatin suppression. In a previous study, they examined the difference in skeletal muscle gene expression between wild type and transgenic mice overexpressing myostatin prodomain (MSTN-pro) using microarray analysis. They observed an overexpression of many myofibrillar protein genes as well as changes in genes involved in various cellular processes were in the transgenic mice. The most significant change in gene expression was the 32-fold overexpression of metallothionein 3 gene in transgenic mice. As a continuation of the previous study, they have examined the global gene expression of hypertrophic muscles induced by beta-adrenergic agionist treatment (clenbuterol) both in wild type and MSTN-pro transgenic mice. Female B6SJL F1 mice were mated to heterozygous MSTN-pro transgenic male mice to produce heterozygous MSTN-pro transgenic mice and wild type (WT) littermate. Pups were weaned at 28 days, then males and females were housed separately and genotype was determined by PCR analysis. At 35 days of age, both MSTN-pro and WT male mice were randomly divided into two groups. The two groups were received 0 ppm or 20 ppm clenbuterol in drinking water for three days, then sacrificed by CO2 asphyxiation, and gastrocnemius, plantaris, soleus, and extensor digitorum longus (EDL) muscles of the lower hind leg were rapidly dissected out, weighed, snap-frozen in liquid nitrogen and stored at -80°C until analysis. Regardless of genotype, clenbuterol significantly increased the weights of the above skeletal muscles. No significant interaction of clenbuterol and genotype effect on skeletal muscle was observed. RNA samples of the gastrocnemius muscle from the clenbuterol-fed WT and clenbuterol-treated MSTN-pro groups were subjected to microarray analysis using the Affymetrix GeneChip Mouse 430-2.0 platform (four chips in each group). Currently, microarray data are being analyzed to identify genes or gene groups differentially expressed by the treatment of beta agonist, clenbuterol and myostatin suppression. The Illinois Station presented their studies in myostatin null mice receiving clenbuterol (clen) treatment. They used clenbuterol mixed in water with 20 ppm clen to male mice for 14 days. Mice were sacrificed at 7 weeks of age for dissection and proximate composition determinations. There was a significant (P<0.05) effect of both clen treatment and genotype but no significant interaction, meaning that wild type and Mstn null mice responded similarly to clen treatment. Body weight, average daily gain, and empty carcass (without skin, head, tail, and viscera) weight were all increased with clen treatment and were greater in Mstn null mice than wild type. Carcass protein percentage was increased with clen treatment and was greater in Mstn null mice, while both visceral and carcass fat percentages were decreased with clen treatment and in Mstn null mice compared with wild type. Furthermore, weights of the retroperitoneal and epididymal fat pads were decreased in Mstn null mice compared with wild type. Epididymal fat pad weight was also decreased by clen treatment. Therefore, they concluded that Mstn null mice do respond to clen treatment and the effects of the Mstn null mutation (increased muscle mass, decreased fat mass) are additive to the effects of clen treatment (increased muscle mass, decreased fat mass). Another project is high fat diet-induced obesity in myostatin null mice. Alterations in myostatin function (Mstn null, transgenic overexpression of Mstn propeptide) result in decreased adiposity and resistance to fat gain. Combining the Mstn null mutation with either the leptin ob/ob mutation or the Agouti yellow mutation reduced obesity and normalized glucose levels. In their study, they fed high (60% calories from fat) or a low (10% calories from fat) diets to wild type and Mstn null mice from 4-16 weeks of age. At 16 weeks of age, were sacrificed and dissected and tissues were saved for further analysis. Body weight, measured weekly, differed by dietary treatment starting in week 1 of the study and by genotype starting in week 2 of the study. At week 6, the interaction of genotype and dietary treatment was trending towards significance (P = 0.15). Blood glucose levels following glucose bolus differed by dietary treatment but not genotype. Genotype and dietary treatment significantly impacted carcass weight, weights of several fat pads and muscles. The Indiana Station studied the regulation of satellite cell function by notch signaling in the skeletal muscle. The group is particularly interested in the signaling pathways that regulate the cell fate choice between self-renewal and differentiation in activated satellite cells. To this end, they have a mouse model to investigate the regulation of satellite cell fate by an evolutionary conserved signaling transduction pathway-the Notch signaling. In this transgenic mouse model, the Notch signaling can be visualized as it exhibits green fluorescence (GFP). The self-renewal and differentiation of satellite cells were dissected using in vitro single myofiber culture and in vivo muscle regeneration models, in which self-renewal and differentiating progenies can be readily identified with specific markers. They discovered an unexpected heterogeneity and dynamics in Notch activation in both quiescent and activated satellite cells. They have also established a strategy to purify satellite cells exhibiting Notch signaling and analyzed their gene expression profiles. Phenotypic heterogeneities have been documented in satellite cells derived from slow and fast muscles. However, the intrinsic molecular mechanisms are unknown due to technical difficulties in isolating fiber type-specific satellite cells. The group has initiated a project to explore the intrinsic molecular mechanisms that program the developmental fate of satellite cells and restrict them to a specific muscle fiber type. They have established unique mouse models that express cyan and red fluorescent proteins in the type I slow and type IIa fast fibers, respectively. These mice provide an unprecedented opportunity to isolate fresh satellite cells from these specific cohorts of fibers and investigate their unique gene expression patterns by high throughput microarray or illumina array analysis. This project will form a foundation for their long-term goal of understanding the molecular regulation of muscle development and growth. Another project is to assess the role of AMPK in metabolism of growing pigs. The purpose of this study was to determine the effect of long-term administration of 5-aminoimidazole-4-carboxamide-1-D-ribofuranoside (AICAR), a known activator of the energy sensor 5'-AMP-activated protein kinase (AMPK), on energy metabolism and myosin heavy chain (MyHC) isoform expression in growing pigs. AICAR treatment caused a significant decrease in mRNA and protein levels of type IIa MyHC isoform and a concomitant increase in type IIx fibers. Consistent with MyHC isoform shift from IIa to IIx, muscles from pigs treated with AICAR showed increased expression and activity of lactate dehydrogenase (LDH), which is an enzyme responsible for anaerobic glycolysis. However, AICAR administration did not alter expression of PPAR³ coactivator (PGC)-1±, fatty acid translocase (FAT/CD36), citrate synthase, or the activity of cytochrome c oxidase (COX). Overall, these results suggest that activation of AMPK by AICAR increases glycolytic capacity by increasing MyHC IIx isoform and increasing LDH activity. The signal transduction cascades that maintain muscle mass remain somewhat obscure but important to animal growth. They have been investigating the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling and have shown that inhibition of this pathway in vitro decreases myotube size and protein content after 3d treatment with a MEK inhibitor. Neither p38 nor JNK inhibitors had any effect on myotube size or morphology. ERK1/2 inhibition also up-regulated gene transcription of atrogin-1 and MuRF-1, and down-regulated the phosphorylation of Akt and its downstream kinases. Forced expression of EGFP-tagged MAPK phosphatase-1 (MKP1) in soleus and gastrocnemius muscles decreased both fiber size and reporter activity. This atrophic effect of MKP1 was time-dependent. Analysis of the reporter activity in vivo revealed that the activities of nuclear factor kappa B (NF-kB) and 26S ribosome were differentially activated in slow and fast muscles, suggesting muscle type-specific mechanisms may be utilized. Together, these findings suggest that MAPK signaling is necessary for the maintenance of skeletal muscle mass as inhibition of these signaling cascades elicits muscle atrophy in vitro and in vivo. Skeletal troponin (Tn) exchange is a good model to use to develop methods to study protein dissociation kinetics from the isolated myofibril. The group showed that troponin's dissociation rate is regulated by calcium and strong (rigor) crossbridges. These different rates fit well with the three-state model (B<->C<->M) of the thin filament for regulation of contraction and are well explained by changes in Tn domain interactions within Tn and between Tn domains and actin-tropomyosin. More recently, they investigated the difference between cardiac and fast skeletal Tn isoforms (in skeletal myofibrils) by measuring the Tn dissociation rate and the pCa-ATPase relationship. They observe three different dissociation rates for both isoforms, but there are large differences in the rates between the two isoforms. In general, the cardiac isoform has a faster dissociation rate under all conditions, is more sensitive but less cooperative in terms of calcium enhanced Tn dissociation rate, and is less in the B or off state in the absence of calcium. The observed differences in the pCa-ATPase activity relationship further support these observations. These studies suggest that three-state equilibrium of the thin filament is dependent upon Tn isoform. Their current studies use ionic strength to alter the equilibrium between the three states. Biochemical studies using reconstituted thin filaments and myosin S1 suggested that low ionic strength, in the absence of free calcium, shifts the equilibrium away from the B or off state and into the C and/or M state. They measured Tn dissociation rate and ATPase activity of myofibrils at different ionic strengths to determine if these conditions influence the three-state equilibrium in a more physiologically intact system. Low ionic strength (25- 50 mM) increases Tn dissociation rate and ATPase activity in the absence of calcium. Also, the ATPase activity is more sensitive and cooperative to activation by calcium at low compared to high ionic strength. Studies to define the molecular mechanism use myofibrils with TnIT exchanged for Tn to give a constitutive B or off state myofibril. Preliminary data suggest that the low ionic strength effects are only partially (30%) mediated by TnI. Addition of TnC to the TnIT myofibrils suggests that TnC is required for the full, low ionic strength effects on the thin filament. Future studies will investigate structural protein dissociation rates to determine if they limit protein turnover rates. The Ohio Station updated their research on the role of the extracellular matrix in avian skeletal muscle development. Current research efforts are focused on understanding the mechanism of how the heparan sulfate family of proteoglycans may be involved in the regulation of muscle growth properties. Fibroblast growth factor 2 (FGF2) is a potent stimulator of muscle cell proliferation and a strong inhibitor of muscle cell differentiation. Heparan sulfate proteoglycans function as a low affinity receptor for FGF2 thus permitting a high affinity interaction of FGF2 with its receptor. Their research is focused on the heparan sulfate proteoglycan syndecan and glypican families. By using a site directed mutagenesis approach the glycosaminoglycan attachment sites were mutated to create a series of site directed mutants for glypican-1 and syndecan-4. For glypican-1, the GAG attachment sites at Ser483, Ser485, and Ser487 were mutated to threonine to obtain 1-chain and no-chain mutants. A similar approach was done for syndecan-4 mutating serine sites 38, 65, and 67. The various constructs of syndecan-4 and glypican-1 were transfected into turkey satellite cells to assay the effect of the GAG chains on the proliferation, differentiation, and responsiveness to FGF2. The data obtained for glypican-1 suggests that glypican-1 function requires the GAG chain attachment sites for myogenic satellite cell FGF2 responsiveness during proliferation and to affect the process of differentiation. In contrast syndecan-4 may affect satellite cell behavior independent of the attached GAG chains and function in a manner independent of FGF2. Also attached to the proteoglycan core protein are N-glycosylation chains. The function of the glycosylated chains has not been well studied to date. To begin to address the function of the N-glycosylation chains a site directed mutagenesis approach was used to create all possible N-glycan chain combinations and a no-chain construct. Preliminary data for both glypican-1 and syndecan-4 suggests that the N-glycan chains do not affect satellite cell proliferation, but differentiation is affected by the absence of the N-glycan chains attached to the core protein. The absence of the N-glycan chains increases differentiation for glypican-1 and in contrast differentiation is decreased by the absence of N-glycan chains for syndecan-4. The second project in Ohio station is the role of transforming growth factor beta1 signaling. Transforming growth factor-beta1 (TGF-beta1) induces apoptosis in many cell types. The cell adhesion receptor, beta1 integrin subunit, prevents apoptosis and may be involved in TGF-beta1-induced muscle cell apoptosis. Chicken primary satellite cells were used to investigate the apoptotic effect of TGF-beta1 on muscle cells. The data showed that the addition of exogenous TGF-beta1 reduced beta1 integrin expression and altered its localization. Treatment of the satellite cells with TGF-beta1 increased the number of apoptotic cells and increased the number of caspase positive cells. Expression of the anti-apoptotic gene Bcl-2 was significantly reduced by TGF-beta1. These data suggest that the apoptotic effect of TGF-beta1 on satellite cells was likely associated with a beta1 integrin-mediated signaling pathway. The Minnesota station studied the roles of IGF-I and the estrogen, androgen and IGF-I receptors in estradiol-17beta and trenbolone acetate- stimulated proliferation of cultured bovine satellite cells. A combined estradiol 17beta (E2)/trenbolone acetate (TBA) implant causes a significant increase in muscle IGF-I mRNA and both E2 and TBA stimulate a significant increase in IGF-I mRNA level in bovine satellite cell (BSC) cultures in media containing 10% fetal bovine serum (FBS). Consequently, increased IGF-I expression may play a role in anabolic steroid enhanced muscle growth. However, even though treatment of cultured BSC with E2 or TBA in media containing 1% IGFBP-3-free swine serum (SS) results in increased proliferation there is no effect on IGF-I mRNA expression, suggesting that increased IGF-I expression may not be responsible for anabolic steroid enhanced BSC proliferation. To further examine the role of estrogen, androgen and IGF-I receptors and their respective ligands in E2 and TBA-stimulated BSC proliferation, the Minnesota group assessed the effects of specific inhibitors on E2 or TBA-stimulated proliferation of BSC. Both ICI 182 780 (an estrogen receptor blocker) and flutamide (an inhibitor of androgen receptor) suppressed (p<0.05) E2 and TBA-stimulated BSC proliferation, respectively. JB1 (a competitive inhibitor of IGF-I binding to type I IGF receptor) reduced (p<0.05) both E2 and TBA-stimulated proliferation in BSC cultures. Both the Raf-1/MAPK kinase (MEK)1/2/ERK1/2, and the phosphatidylinositol 3-kinase (PI3K)/Akt pathways play significant roles in the actions of IGF-I on proliferation and differentiation of myogenic cells. PD98059, an inhibitor of the MAPK pathway, and wortmannin, and inhibitor of the PI3K pathway, both suppressed (p<0.05) E2 and TBA-stimulated proliferation of cultured BSC. Their data suggest that IGF-I plays a role in E2 and TBA stimulated proliferation of cultured BSC even in the absence of increased IGF-I expression. The second project in this station is to study the potential role of G-protein-coupled receptor 30 (GPR30) in estradiol-17beta-stimulated IGF-I mRNA expression in bovine satellite cell cultures. Androgenic and estrogenic steroids enhance muscle growth in animals and humans. Estradiol-17beta (E2) and trenbolone acetate (TBA) (a synthetic testosterone analog increased IGF-I mRNA expression in bovine muscle satellite cell (BSC) cultures. The goal of this study was to evaluate the mechanisms responsible for this increase by evaluating the effects of ICI 182 780 (an E2 receptor antagonist), flutamide (an androgen receptor inhibitor), G1 (a GPR30 agonist), and BSA-conjugated E2 on E2 and/or TBA-stimulated IGF-I mRNA expression in BSC cultures. Flutamide completely suppressed TBA-stimulated IGF-I mRNA expression in BSC cultures. ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced (93%, p < 0.05) IGF-I mRNA levels in BSC cultures. G1 (100 nM) stimulated IGF-I mRNA expression (100%, p < 0.05) but had no effect on proliferation in BSC cultures. E2-BSA, which cannot cross the cell membrane, stimulated IGF-I mRNA expression (approximately 100%, p < 0.05) in BSC but even at extremely high concentrations had no effect on proliferation. In summary, their data indicate the E2-stimulation of proliferation and E2-stimulation of IGF-I mRNA expression in BSC cultures occur via different mechanisms. Stimulation by ICI 182 780, G1 and E2-BSA suggests the E2-stimulated IGF-I mRNA expression in BSC cultures is mediated through the GPR30 receptor. The third project is to examine the effects of trenbolone acetate (TBA), estradiol (E2) and combined TBA/E2 implants on muscle IGF-I, IGF-I receptor, estrogen receptor-± and androgen receptor mRNA levels in feedlot steers. They have previously shown that a combined trenbolone acetate (TBA)/ estradiol-17beta (E2) implant significantly increases IGF-I mRNA levels in longissimus dorsi (LD) muscles of feedlot steers by 28 days after implantation. Here they compare the effects of E2 (25.7 mg), TBA (120 mg) and combined /TBA (120 mg)/ E2 (24 mg) implants on IGF-I, IGF-I receptor (IGFR-1), estrogen receptor (ER)-± and androgen receptor (AR) mRNA levels in the LD muscles of steers implanted for 28 days. Five yearling steers per group were implanted with each implant and 5 control steers received no implant. Steers were weighed weekly starting on d 0 and muscle biopsy samples were taken from each steer on d 0 (prior to implantation), d 7, d 14 and d 28. RNA was prepared from each sample and real-time RT-PCR was used to determine the levels of IGF-I, IGFR-1, ER-± and AR mRNA. Body weight of implanted steers tended (P = 0.09) to be greater than that of CTL steers. On d 7 and 28 IGF-I mRNA levels were higher (58% and 78%, respectively) (p < 0.009) in E2 implanted animals than in control steers. Similarly, on d 28 the LD muscle IGF-I mRNA level was 65% higher (P = 0.017) in TBA/E2 implanted steers than in control animals. In contrast, the TBA implant did not increase LD muscle IGF-I mRNA levels after 28 days of implantation. These data suggest that E2 is responsible for the increased muscle IGF-I mRNA level observed in steers implanted with a combined TBA/E2 implant. The Texas Station utilizes a unique cattle population for investigation of differential gene expression and signal transduction in skeletal muscle resulting from inheritance of Bos taurus or Bos indicus alleles. This project uses microarray, quantitative realtime RT-PCR, and proteomic analyses of skeletal muscle from steers to characterize the Brahman influence on carcass traits and meat characteristics. In addition, expression profiles will be correlated to extensive phenotype, SNP and QTL data from this population of animals. Genetic mechanisms influencing these complex traits remain poorly understood. One objective of the McGregor Genomics Project is to identify potentially valuable QTL for use in breeding programs for a variety of these traits. Approximately 180 F2 Nellore-Angus steers were assessed for feed efficiency as determined by computation of model predicted residual consumption (MPRC). Animals with the greatest positive or smallest negative MPRC values were identified as least efficient or most efficient, respectively. The Texas group extracted RNA from skeletal muscle from the 14 most efficient and 14 least efficient animals for microarray analysis. They used data generated from Agilent bovine oligo microarrays to identify candidate genes for further study. Among differentially expressed genes verified between the two groups, ±-actinin 3 (ACTN3), was expressed nearly 3-fold higher in the inefficient group when compared to the efficient group. ACTN3 is expressed only in fast twitch muscle fibers. Actinins are myofilament proteins essential to Z-line attachment for actin fibers, and have been shown to bind factors relating to myofiber differentiation as well as muscle contraction. The Washington station characterized selected signal transduction pathways that regulate skeletal muscle growth and differentiation. Skeletal muscle is composed of a variety of cells, including adipocytes. For a considerable number of years the Washington station have been interested in the mechanism of intercellular communication between muscle cells and intramuscular adipocytes. During an attempt to develop a defined co-culture system, it was obvious that 3T3-L1 cells and stromal vascular cells were not sufficiently defined to use as the adipocyte cell component of the defined co-culture system. As such, they looked for an alternative adipocyte, which could be used in our developing system. The group devised repeatable methods to isolate mature adipocytes from beef cattle and to generate progeny cultures of adipofibroblasts for use in a variety of studies. Whereas beef-derived (mature) adipocytes retained lipid and divided in an asymmetric or symmetric manner, similar cells from pigs had to physically extrude lipid from the cell prior to proliferation. Another project is to determine molecular mechanisms that control gene expression in skeletal muscle. The group has previously shown that mature lipid-filled beef-derived adipocytes possess the ability to return to a proliferative-competent state and produce progeny cells. Such progeny cells have been tested for numerous properties, and compared to 3T3-L1 and stromal vascular cells. Bovine-specific oligo microarrays and qRT-PCR were used to determine differentially expressed genes in purified progeny cultures of dedifferentiated beef-derived (mature) adipocytes and to validate selected genes considered closely associated with adipogenesis. The same methods were used to compare differentially expressed genes in subcutaneous adipose tissues of beef steers with different backfat thickness. A variety of intrinsic factors were different between proliferative vs redifferentiative adipofibroblasts, and between individuals of the same breed (developmental study) and between two cattle crossbreds (direct comparison study). The Wisconsin Station characterized a mutation that affects alternative splicing of titin. An autosomal dominant mutation that dramatically alters the alternative splicing pattern of titin has been described (Greaser et al., J. Mus. Res. & Cell Motil 26:325-332, 2005). In spite of the dramatic change in titin size, the animals remain visibly healthy. Electron micrographs of homozygous mutant ventricles showed occasional regions of myofibrillar disarray. The mutants also contained unusual clustering of mitochondria and often had very wide myofibrils. Changes in cardiac muscle transcriptional levels from mutant compared to normal rat ventricular were determined using Affymetrix Rat 230 2.0 microarrays. Results showed that 433 genes (from a total of 31099) were differentially expressed in mutant compared to normal rats. 239 genes were down-regulated and 194 genes were differentially up-regulated. Genes that exhibited the largest increase in expression were sarcomeric proteins and regulation of muscle contraction, G-protein signaling and calcium regulation in cardiac cells. The other project is to study the role of phosphorylation in myosin binding protein C function. Normal cardiac function requires dynamic modulation of contraction. Beta1-adrenergic-induced protein kinase A (PKA) phosphorylation of cardiac myosin binding protein (cMyBP)-C may regulate crossbridge kinetics to modulate contraction. The group tested this idea with mechanical measurements and echocardiography in a mouse model lacking 3 PKA sites on cMyBP-C, ie, cMyBP-C(t3SA). They developed the model by transgenic expression of mutant cMyBP-C with Ser-to-Ala mutations on the cMyBP-C knockout background. Western blots, immunofluorescence, and in vitro phosphorylation combined to show that non-PKA-phosphorylatable cMyBP-C expressed at 74% compared to normal wild-type (WT) and was correctly positioned in the sarcomeres. Similar expression of WT cMyBP-C at 72% served as control, ie, cMyBP-C(tWT). Skinned myocardium responded to stretch with an immediate increase in force, followed by a transient relaxation of force and finally a delayed development of force, ie, stretch activation. The rate constants of relaxation, k(rel) (s-1), and delayed force development, k(df) (s-1), in the stretch activation response are indicators of crossbridge cycling kinetics. cMyBP-C(t3SA) myocardium had baseline k(rel) and k(df) similar to WT myocardium, but, unlike WT, k(rel) and k(df) were not accelerated by PKA treatment. Reduced dobutamine augmentation of systolic function in cMyBP-C(t3SA) hearts during echocardiography corroborated the stretch activation findings. Furthermore, cMyBP-C(t3SA) hearts exhibited basal echocardiographic findings of systolic dysfunction, diastolic dysfunction, and hypertrophy. Conversely, cMyBP-C(tWT) hearts performed similar to WT. Thus, PKA phosphorylation of cMyBP-C accelerates crossbridge kinetics and loss of this regulation leads to cardiac dysfunction. The Wyoming Station continues their work on AMPK and skeletal muscle growth and growth. The group studied the role of AMPK in the regulation of skeletal muscle development. They found that AMPK controls the skeletal muscle development through sensitizing the insulin/insulin-like growth factor-1 signaling. In C2C12 myoblast cell culture, they also demonstrated that Ca2+/calmodulin-dependent protein kinase kinase is involved in the activation of AMPK, linking calcium signaling, AMPK and skeletal muscle growth. Currently, they are further investigating the role of AMPK in skeletal muscle growth by employing RN- pigs which carries a mutation in muscle-specific AMPK g3 subunit. They are also investigating the role of AMPK in muscle growth and development using a transgenic mice which carry a R225Q mutation in AMPKg3 subunit, corresponding to the mutation in RN- pigs. In addition, the group is investigating the role of AMPK in fetal muscle development. Since meat animals spend one third to half of their lives in utero, muscle development during fetal stage is essential for growth performance of offspring. Therefore, studies on the association between maternal nutrition and fetal skeletal muscle development are very important. Another project is to define the role of AMPK in the marbling of beef cattle. AMPK has a key role in the regulation of marbling. AMPK activity in skeletal muscle is negatively associated with marbling in beef cattle. Data suggested that nutrition during fetal stage is closely associated with marbling in beef cattle and lamb. The group showed that nutrient supplementation during gestation in the dam enhanced marbling in fetal muscle. They are currently studying the myogenesis and adipogenesis from mesenchymal stem cells. Their studies show that AMPK is involved in muscle growth, postmortem glycolysis and marbling. It is known that selection of animals for enhanced muscle growth increases incidence of PSE meat, and also reduces marbling in livestock. But the underlying mechanisms remain undefined. Their studies suggest that AMPK participates in all these three aspects providing a possibly explanation for such negative association between muscle growth and meat quality.

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