Comparison of the foetal development of muscle in normal and double-muscled cattle

Picard, Brigitte; Gagnière, Hélène; Robelin, J.; Geay, Y.

doi:10.1007/bf00130244

Cited by 31 publications

(22 citation statements)

References 21 publications

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“…This result was consistent with the pattern of expression of myosin isoforms observed by immunocytochemical detection, indicating the presence of more mature myosins in the muscles of normal than of double-muscled foetuses at the same gestational stage [6]. These observations confirm a delay in the degree of differentiation of double-muscled foetuses.…”

Section: Discussionsupporting

confidence: 89%

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Growth hormone receptor gene expression in the skeletal muscle of normal and double-muscled bovines during foetal development

Listrat

Hocquette²,

Picard³

et al. 2005

Reprod. Nutr. Dev.

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-The expression of the growth hormone receptor (GHR) gene was investigated in semitendinosus muscle during bovine foetal development in both normal and double-muscled Charolais foetuses which differ with respect to muscle development. Northern-blot analysis of foetal muscle RNA preparations with a GHR cDNA probe identified the 4.5 kb GHR mRNA as early as 130 days post-conception. In double-muscled animals, the expression of GHR mRNA increased from 130 to 210 days of gestation while it stayed stable in normal ones. It was significantly higher (P < 0.05) in double-muscled foetuses compared to normal ones from the second third of gestation. Northern-blot analysis of foetal muscle RNA preparations from both genotypes with a β-actin cDNA probe, revealed lower β-actin gene expression in double-muscled foetuses than in normal ones, suggesting a delay in the differentiation of muscle cells. In situ hybridisation revealed the localisation of specific GHR mRNA in muscle cells at all gestation stages analysed (130, 170, 210 days postconception) but not in connective tissue surrounding the muscle cells. At the adult stage, the hybridisation signal was also very high and observed in muscle cells only. These results show the ontogeny of GHR mRNA in bovine muscle and demonstrate a difference between normal and doublemuscled animals. muscle / bovine / receptor / growth hormone / in situ hybridisation

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Section: Discussionsupporting

confidence: 89%

“…The hypertrophy of some superficial muscles, which results from the presence of inactive myostatin, is the consequence of an increase in the total fibre number [2] due to hyperplasia [3,4]. Picard et al [5,6] showed, in vivo and in vitro, that there was a variable delay in contractile differentiation of the 394 A. Listrat et al…”

Section: Introductionmentioning

confidence: 99%

Growth hormone receptor gene expression in the skeletal muscle of normal and double-muscled bovines during foetal development

Listrat

Hocquette²,

Picard³

et al. 2005

Reprod. Nutr. Dev.

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“…This was accompanied by a reduced adipocyte hypertrophy with no effect on their number, and a decreased lipogenesis in WAT. In muscle, energy restriction from birth to weaning decreased cross-section area and increased the proportion of fast glycolytic fibres, which were not detectable at slaughter (Picard et al, 1995). Although the increase in lean-to-fat ratio at weaning is spectacular, it is generally less marked when slaughter occurs later, depending on the feeding following weaning (Berge et al, 1991;Greenwood and Cafe, 2007).…”

Section: Nutritional and Physiological Control Of Muscular And At Growthmentioning

confidence: 99%

Ontogenesis of muscle and adipose tissues and their interactions in ruminants and other species

Bonnet

Cassar-Malek

Chilliard

et al. 2010

Animal

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110

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The lean-to-fat ratio, that is, the relative masses of muscle and adipose tissue, is a criterion for the yield and quality of bovine carcasses and meat. This review describes the interactions between muscle and adipose tissue (AT) that may regulate the dynamic balance between the number and size of muscle v. adipose cells. Muscle and adipose tissue in cattle grow by an increase in the number of cells (hyperplasia), mainly during foetal life. The total number of muscle fibres is set by the end of the second trimester of gestation. By contrast, the number of adipocytes is never set. Number of adipocytes increases mainly before birth until 1 year of age, depending on the anatomical location of the adipose tissue. Hyperplasia concerns brown pre-adipocytes during foetal life and white pre-adipocytes from a few weeks after birth. A decrease in the number of secondary myofibres and an increase in adiposity in lambs born from mothers severely underfed during early pregnancy suggest a balance in the commitment of a common progenitor into the myogenic or adipogenic lineages, or a reciprocal regulation of the commitment of two distinct progenitors. The developmental origin of white adipocytes is a subject of debate. Molecular and histological data suggested a possible transdifferentiation of brown into white adipocytes, but this hypothesis has now been challenged by the characterization of distinct precursor cells for brown and white adipocytes in mice. Increased nutrient storage in fully differentiated muscle fibres and adipocytes, resulting in cell enlargement (hypertrophy), is thought to be the main mechanism, whereby muscle and fat masses increase in growing cattle. Competition or prioritization between adipose and muscle cells for the uptake and metabolism of nutrients is suggested, besides the successive waves of growth of muscle v. adipose tissue, by the inhibited or delayed adipose tissue growth in bovine genotypes exhibiting strong muscular development. This competition or prioritization occurs through cellular signalling pathways and the secretion of proteins by adipose tissue (adipokines) and muscle (myokines), putatively regulating their hypertrophy in a reciprocal manner. Further work on the mechanisms underlying cross-talk between brown or white adipocytes and muscle fibres will help to achieve better understanding as a prerequisite to improving the control of body growth and composition in cattle.

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“…The properties of DM muscles appear during foetal development (Picard et al, 1995;Deveaux et al, 2001). MSTN expression is detected from 16 days in bovine embryos (Kambadur et al, 1997) and is regulated throughout gestation (Deveaux et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…This is likely to be the consequence of disinhibition of myoblast proliferation at crucial stages of myogenesis (Picard et al, 1998;Thomas et al, 2000;Deveaux et al, 2001). Muscle contractile and metabolic differentiation of DM animals is delayed compared to that of conventional animals (Gagniè re et al, 1997) as their muscles express fewer mature myosin heavy chains at the same gestational age during the first two-thirds of foetal life (Picard et al, 1995;Martyn et al, 2004). However, whether the delay of muscle differentiation is strictly related to the initial difference in proliferation or whether it is related to some other process has not been elucidated yet.…”

Section: Introductionmentioning

confidence: 99%

Myostatin inactivation induces a similar muscle molecular signature in double-muscled cattle as in mice

Chelh

Picard

Hocquette

et al. 2011

Animal

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Myostatin (MSTN), a member of the TGF-b superfamily, is a negative regulator of skeletal muscle mass. We have previously shown that the cell survival/apoptosis pathway is a downstream target of MSTN loss-of-function in mice through the regulation of the expression or abundance of many survival and apoptotic factors. In this study, we used western-blot and quantitative PCR (qPCR) analyses to validate these novel downstream targets of MSTN in double-muscled (DM) cattle v. their controls including 260-day-old foetuses and adult cows from the INRA95 strain. MSTN loss-of-function in DM foetuses and DM cows resulted in a glycolytic shift of the muscles (e.g. upregulation of H-MyBP, PGM1 and SNTA1 and downregulation of H-FABP), activation of cell survival pathway through regulation of some components of the PI3K/Akt pathway (e.g. upregulation of DJ-1 and Gsk-3bser9/ Gsk-3btotal ratio and downregulation of PTEN) and upregulation of cell survival factors translationally controlled tumour protein (14-3-3E, Pink1). We also found a lower abundance of pro-apoptotic transcripts and/or proteins (Caspase-3, caspase-8, caspase-9, BID, ID2 and Daxx) and a higher expression of anti-apoptotic transcripts (Traf2 and Bcl2l2) in DM muscles. All together, these results are in favour of activation of the cell survival pathway and loss of apoptosis pathway within the muscles of DM animals. Alteration of both pathways may increase myonuclear or satellite cell survival, which is crucial for protein synthesis. This could contribute to muscle hypertrophy in DM foetuses and DM cows.Keywords: myostatin, cattle, muscle hypertrophy, apoptosis, cell survival ImplicationsMuscle hypertrophy has been extensively studied in meatproducing animals. In double-muscled (DM) cattle, a loss-offunction mutation in the myostatin gene (MSTN ) is responsible for muscle hypertrophy. In order to get a thorough knowledge of the molecular mechanisms of MSTN action, we have examined the molecular phenotype of DM muscle based on our previous data in MSTN-null mice. The data bring new elements to the understanding of the DM muscle phenotype and of the regulation of muscle mass in farm animals.

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Comparison of the foetal development of muscle in normal and double-muscled cattle

Cited by 31 publications

References 21 publications

Growth hormone receptor gene expression in the skeletal muscle of normal and double-muscled bovines during foetal development

Growth hormone receptor gene expression in the skeletal muscle of normal and double-muscled bovines during foetal development

Ontogenesis of muscle and adipose tissues and their interactions in ruminants and other species

Myostatin inactivation induces a similar muscle molecular signature in double-muscled cattle as in mice

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