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Skeletal muscle wasting, whether related to physiological ageing, muscle disuse or to an underlying chronic disease, is a key determinant to quality of life and mortality. However, cellular basis responsible for increased catabolism in myocytes often remains unclear. Although myocytes represent the vast majority of skeletal muscle cellular population, they are surrounded by numerous cells with various functions. Animal models, mostly rodents, can help to decipher the mechanisms behind this highly dynamic process, by allowing access to every muscle as well as time‐course studies. Satellite cells (SCs) play a crucial role in muscle regeneration, within a niche also composed of fibroblasts and vascular and immune cells. Their proliferation and differentiation is altered in several models of muscle wasting such as cancer, chronic kidney disease or chronic obstructive pulmonary disease (COPD). Fibro‐adipogenic progenitor cells are also responsible for functional muscle growth and repair and are associated in disease to muscle fibrosis such as in chronic kidney disease. Other cells have recently proven to have direct myogenic potential, such as pericytes. Outside their role in angiogenesis, endothelial cells and pericytes also participate to healthy muscle homoeostasis by promoting SC pool maintenance (so‐called myogenesis–angiogenesis coupling). Their role in chronic diseases muscle wasting has been less studied. Immune cells are pivotal for muscle repair after injury: Macrophages undergo a transition from the M1 to the M2 state along with the transition between the inflammatory and resolutive phase of muscle repair. T regulatory lymphocytes promote and regulate this transition and are also able to activate SC proliferation and differentiation. Neural cells such as terminal Schwann cells, motor neurons and kranocytes are notably implicated in age‐related sarcopenia. Last, newly identified cells in skeletal muscle, such as telocytes or interstitial tenocytes could play a role in tissular homoeostasis. We also put a special focus on cellular alterations occurring in COPD, a chronic and highly prevalent respiratory disease mainly linked to tobacco smoke exposure, where muscle wasting is strongly associated with increased mortality, and discuss the pros and cons of animal models versus human studies in this context. Finally, we discuss resident cells metabolism and present future promising leads for research, including the use of muscle organoids.

Beta‐alanine (BA) supplementation increases muscle carnosine, an abundant endogenous antioxidant and pH buffer in skeletal muscle. Carnosine loading promotes exercise capacity in healthy older adults. As patients with chronic obstructive pulmonary disease (COPD) suffer from elevated exercise‐induced muscle oxidative/carbonyl stress and acidosis, and from reduced muscle carnosine stores, it was investigated whether BA supplementation augments muscle carnosine and induces beneficial changes in exercise capacity, quadriceps function, and muscle oxidative/carbonyl stress in patients with COPD. In this double‐blind, randomized, placebo (PL)‐controlled trial (clinicaltrials.govidentifier: NCT02770417), 40 patients (75% male) with COPD (mean ± standard deviation: age 65 ± 6 years; FEV1% predicted 55 ± 14%) were assigned to 12 weeks oral BA or PL supplementation (3.2 g/day). The primary outcome, i.e. muscle carnosine, was quantified from m. vastus lateralis biopsies obtained before and after intervention. Co‐primary outcomes, i.e. incremental and constant work rate cycle capacity, were also assessed. Linear mixed model analyses were performed. Compliance with and side effects of supplement intake and secondary outcomes (quadriceps strength and endurance, and muscle oxidative/carbonyl stress) were also assessed. Beta‐alanine supplementation increased muscle carnosine in comparison with PL in patients with COPD (mean difference [95% confidence interval]; +2.82 [1.49–4.14] mmol/kg wet weight; P< 0.001). Maximal incremental cycling capacity (VO2peak: +0.5 [−0.7 to 1.7] mL/kg/min; P= 0.384, Wpeak: +5 [−1 to 11] W; P= 0.103) and time to exhaustion on the constant work rate cycle test (+28 [−179 to 236] s; P= 0.782) did not change significantly. Compliance with supplement intake was similar in BA (median (quartile 1–quartile 3); 100 (98–100)%) and PL (98 (96–100)%) (P= 0.294) groups, and patients did not report side effects possibly related to supplement intake. No change was observed in secondary outcomes. Beta‐alanine supplementation is efficacious in augmenting muscle carnosine (+54% from mean baseline value) without side effects in patients with COPD in comparison with PL. However, accompanied beneficial changes in exercise capacity, quadriceps function, and muscle oxidative/carbonyl stress were not observed.

Des recherches récentes explorent ce que les plateformes digitales font et font faire aux utilisateurs. Dans leur prolongement, cet article étudie comment les plateformes digitales P2P accélèrent les activités marchandes, et comment cette accélération modèle les relations entre utilisateurs. Une étude qualitative à caractère ethnographique a été menée au sein du marché des vêtements d’occasion de 2013 à 2020. En mobilisant la théorie de l’accélération sociale, nous montrons que les affordances des plateformes digitales encouragent une accélération du rythme de vie, une accélération du renouvellement des objets possédés, et une accélération technique multi-domaines. Ces formes d’accélération aboutissent à une concurrence par la rapidité entre utilisateurs : chacun d’eux se doit d’être plus réactif, plus à la pointe, et plus averti que les autres. De plus, les plateformes constituent un espace digital particulier qui invite à repenser l’aliénation sous plusieurs formes, et notamment l’aliénation par rapport à l’espace et par rapport au temps. Outre ses contributions théoriques, cette recherche offre des contributions sociétales visant à faire prendre conscience aux utilisateurs de l’ampleur de leurs activités marchandes accélérées sur les plateformes digitales.

A good knowledge of the genome properties of the populations makes it possible to optimize breeding methods, in particular genomic selection (GS). In oil palm (Elaeis guineensisJacq), the world’s main source of vegetable oil, this would provide insight into the promising GS results obtained so far. The present study considered two complex breeding populations, Deli and La Mé, with 943 individuals and 7324 single-nucleotide polymorphisms (SNPs) from genotyping-by-sequencing. Linkage disequilibrium (LD), haplotype sharing, effective size (Ne), and fixation index (Fst) were investigated. A genetic linkage map spanning 1778.52 cM and with a recombination rate of 2.85 cM/Mbp was constructed. The LD at r2=0.3, considered the minimum to get reliable GS results, spanned over 1.05 cM/0.22 Mbp in Deli and 0.9 cM/0.21 Mbp in La Mé. The significant degree of differentiation existing between Deli and La Mé was confirmed by the high Fstvalue (0.53), the pattern of correlation of SNP heterozygosity and allele frequency among populations, and the decrease of persistence of LD and of haplotype sharing among populations with increasing SNP distance. However, the level of resemblance between the two populations over short genomic distances (correlation of rvalues between populations >0.6 for SNPs separated by <0.5 cM/1 kbp and percentage of common haplotypes >40% for haplotypes <3600 bp/0.20 cM) likely explains the superiority of GS models ignoring the parental origin of marker alleles over models taking this information into account. The two populations had low Ne(<5). Population-specific genetic maps and reference genomes are recommended for future studies.

Cette étude visait à améliorer l’élimination des micropolluants en modifiant les conditions de fonctionnement du procédé boues activées à aération prolongée. Cette question a nécessité de mesurer les coefficients de sorption et les constantes de biodégradation (étude pilote), et de décrire la variabilité des concentrations dans les eaux usées brutes et les boues d’une installation en grandeur réelle. 53 micropolluants ont été étudiés (11 métaux et 42 substances organiques). Au total, huit campagnes d’échantillonnage de quelques jours ont été réalisées sur une durée d’un an, pour différentes conditions de fonctionnement de l’installation (concentration en boue, durée de présence d’oxygène, température). Les concentrations dans les eaux usées brutes ont varié de façon importante pour les substances organiques (50 à 100 %), mais moindre pour les métaux (30 %). Au cours d’une période de 24 heures, des concentrations deux fois plus élevées ont été mesurées dans la journée (6 h à 24 h), par comparaison aux concentrations mesurées la nuit pour plusieurs substances (ex. : zinc, plomb, nonylphénol, propranolol, diclofénac).Nous avons démontré que la biodégradation explique l’élimination d’une dizaine de substances (ex. : paracétamol, acébutolol, aténolol, ibuprofène, nonyl- et octyl-phénol). La sorption seule explique le transfert dans les boues des HAP lourds et des métaux. La sorption et la biodégradation expliquent conjointement l’élimination d’une dizaine d’autres substances (ex. : propranolol et quelques HAP). En complément, nous avons démontré que la biodégradation se déroule principalement en condition aérobie, surtout en présence simultanée de DCO et d’azote ammoniacal dans le bioréacteur, et avec une vitesse moindre en présence d’azote seul et très faible en phase endogène. Nous avons mesuré une faible dégradation des micropolluants une fois adsorbés sur les boues (< 10 %).Le modèle ASM1-MIP a été élaboré pour le procédé étudié, et ses prévisions représentent l’évolution temporelle des concentrations mesurées en sortie de STEU, en prenant en compte la variabilité des concentrations. Son utilisation a permis d’évaluer l’impact de l’augmentation de la concentration en boue (pour optimiser la sorption et la biodégradation), d’une plus grande durée d’aération (pour optimiser la biodégradation), et des variations de température. Le modèle prédit que les concentrations de certains micropolluants dans les eaux traitées pourraient être réduites d’au maximum 30 % en modifiant le fonctionnement des boues activées.

We recently generated 2 phenotypically similar Hoxa9+Meis1 overexpressing acute myeloid leukemias that differ by their in vivo biologic behavior. The first leukemia, named FLA2, shows a high frequency of leukemia stem cells (LSCs; 1 in 1.4 cells), whereas the second, FLB1, is more typical with a frequency of LSCs in the range of 1 per several hundred cells. To gain insights into possible mechanisms that determine LSC self-renewal, we profiled and compared the abundance of nuclear and cytoplasmic proteins and phosphoproteins from these leukemias using quantitative proteomics. These analyses revealed differences in proteins associated with stem cell fate, including a hyperactive p38 MAP kinase in FLB1 and a differentially localized Polycomb group protein Ezh2, which is mostly nuclear in FLA2 and predominantly cytoplasmic in FLB1. Together, these newly documented proteomes and phosphoproteomes represent a unique resource with more than 440 differentially expressed proteins and 11 543 unique phosphopeptides, of which 80% are novel and 7% preferentially phosphorylated in the stem cell–enriched leukemia.

Cows are often housed in tie-sheds for some part of the year (from 20 to 80% of adult cows in European countries). By contrast, regulations aiming at improving animal welfare generally provide for more opportunity to express behavior and so limit tethering (the European directive for sows). To inform current debate on whether cows should be tethered from an animal welfare point of view, 2 experiments were conducted to determine whether cows were motivated to walk (if their walking motivation was thwarted by tethering) and whether this frustration resulted in acute or chronic stress. In Exp. 1, fifteen cows were housed in tie-stalls for 1, 3, 9, or 27 d or loose-housed in a pen equipped with free-stalls for 27 d according to a Latin square design. On d 28, cows were observed in an 80-m2arena where they could walk or run for 10 min. In Exp. 2, fifteen cows were either loose-housed or tie-housed with or without 1 h of daily access to an exercise area according to a Latin square design (treatment duration of 27 d). On d 28, cows were observed in the test arena for 10 min as in Exp. 1. In addition, in Exp. 2, milk was sampled twice weekly for cortisol concentrations and cows underwent a chronic stress test (challenge with ACTH, followed by blood samples for cortisol concentrations). When they were tied with no access to exercise, cows displayed a greater locomotor activity in the test arena (time spent walking × 1.4 in Exp. 1, P< 0.05; time spent trotting × 5 in Exp. 2, P< 0.05), whatever the duration of tie-housing. Regular exercise caused locomotor activity in the arena test to revert to levels observed when cows were loose-housed. Basal cortisol concentrations in milk decreased with time whatever the housing condition (P< 0.001). This decrease was more marked when cows were tied than when they were loose-housed (P< 0.05). Cortisol responses to ACTH were similar between treatments. Adult cows are motivated to walk, and tethering thwarts this motivation. However, the frustration produced by tethering does not result in either acute or chronic physiological stress responses. We recommend that cows housed in tie-sheds be given regular access to an exercise area.

In this report, an antisense RNA strategy has allowed us to show that disruption of ALP expression affects the expression of the muscle transcription factors myogenin and MyoD, resulting in the inhibition of muscle differentiation. Introduction of a MyoD expression construct into ALP-antisense cells is sufficient to restore the capacity of the cells to differentiate, illustrating that ALP function occurs upstream of MyoD. It is known that MyoD is under the control of serum response factor (SRF), a transcriptional regulator whose activity is modulated by actin dynamics. A dramatic reduction of actin filament bundles is observed in ALP-antisense cells and treatment of these cells with the actin-stabilizing drug jasplakinolide stimulates SRF activity and restores the capacity of the cells to differentiate. Furthermore, we show that modulation of ALP expression influences SRF activity, the level of its coactivator, MAL, and muscle differentiation. Collectively, these results suggest a critical role of ALP on muscle differentiation, likely via cytoskeletal regulation of SRF.

Multicollector ICP-MS is used for the precise measurement of variations in the isotopic composition of germanium. Argon-based spectral interferences are assessed in the germanium mass region and the repeatability of the following ratios is determined: 74Ge/70Ge, 73Ge/70Ge and 72Ge/70Ge. The isotope ratio repeatability of a mono-elemental solution relative to another mono-elemental solution is better than 0.06‰ per u at 95% confidence. Variations in sample 74Ge/70Ge, 73Ge/70Ge, and 72Ge/70Ge ratios are expressed as δ74Ge δ73Ge and δ72Ge units, respectively, which are deviations in parts per 103 from the same ratio in the standard solution. The addition of sodium and potassium to a standard solution of germanium having a known isotopic composition induces up to 4.4‰ decrease of δ74Ge. This chemical bias is a result of a mass-dependent process and prevents the measurement of natural samples without chemical separation. Germanium is quantitatively separated from alkali matrix using liquid chromatography techniques.

The anti-atherosclerotic properties of F 12511, a novel acyl-coenzyme Acholesterol acyltransferase (ACAT) inhibitor, were studied in rabbits that were fed a cholesterol-free casein-rich diet and developed endogenous hypercholesterolemia and fibrofatty preatheroma lesions. After 6 weeks of casein feeding, an endothelial abrasion was performed in the abdominal aorta; at week 8, a control group was maintained on this diet while F 12511 (8 mg/kg/d) was administered as a diet admixture for the subsequent 24 weeks. Total plasma cholesterol level rose to 250–300 mg/dl in both groups before starting the treatment; F 12511 time-dependently reduced total plasma cholesterol by 50, and also decreased by 50 the incidence of lesions and macrophage accumulation in uninjured aorta (thoracic arch, celiac bifurcation). Residual lesions in the treated group were characterized by few macrophages, essentially under the endothelium, and by a larger content of smooth muscle cells. Quantitative image analysis of serial sections of mechanically injured abdominal aorta revealed a 20 surface covered by preatheroma lesions in the placebo group; F 12511 significantly reduced this surface. These data suggest that the combination of endogenous hypercholesterolemia with endothelial injury in the rabbit may offer a useful model to study atherosclerosis; lipid lowering by F 12511 reduces the incidence of vascular lesions and macrophage infiltration and may reinforce the fibrous skeleton of the atheroma.

The effect of mastitis and related-germs on milk chemical composition (protein and lactose contents) and milk somatic cell count (SCC) was investigated in 501 milk quarter samples during two consecutive years in cows from three experimental herds. Each infected quarter was matched by a healthy one in the same udder, as a control. Milk protein and mineral assays were performed in a sub- sample of 128 milks. Staphylococci were the most frequently isolated germs (Staphylococcus aureus: 27%, coagulase-negative Staphylococci: 26%, Streptococci: 21%). Major milk pathogens (Staphylococcus aureus, Streptococcus uberis or Escherichia coli) associated with clinical signs of mastitis were accompanied by higher SCC (+1.6 log$\cdot$mL$^{-1}$, $P < 0.01$), lower lactose concentration (-7.6 g$\cdot$kg$^{-1}$, $P < 0.01$), higher protein concentration (+3.3 g$\cdot$kg$^{-1}$, $P < 0.01$) and higher soluble protein concentrations (IgG and BSA), hence a sharp decrease in the casein/protein ratio (-10 percentage points, $P < 0.01$). Changes were more marked when Escherichia coli was present. Corynebacterium bovis did not alter milk chemical composition whereas coagulase-negative Staphylococci slightly reduced lactose concentration (-1.8 g$\cdot$kg$^{-1}$) and increased SCC (+0.37 log$\cdot$mL$^{-1}$). Calcium and phosphorus milk contents were hardly modified by the presence of microorganisms. The decrease in milk yield during clinical mastitis varied from 1.6 kg$\cdot$d$^{-1}$ in the presence of Staphylococcus aureus to 15 kg$\cdot$d$^{-1}$ in the presence of Escherichia coli.

Twenty-four multiparous cows were divided into 4 groups immediately after calving according to a 2 $\times$ 2 factorial design: 2 milking frequencies (1 daily [morning only] milking for the first three weeks of lactation, then 2 daily milkings vs. 2 daily milkings throughout) under two diet energy concentrations (normal or low). The trial lasted 30 weeks, on average, and ended in the pasture on 28 May 2000. During the winter period, the cows were housed together in a free-stall barn, and were given complete rations ad libitum. The cows that were not milked were significantly more vocal than the controls, close to the omitted milking, and in a large number of them, milk leaked from the udder. Once-daily milking gradually reduced the amount of milk secreted in relation to that produced by cows milked twice a day, with differences of 8.5 kg$\cdot$d$^{-1}$ ($P < 0.01$) at week 3. As early as the first week of resumption of twice-daily milking, that difference ceased to be statistically significant but amounted to 1.3 kg$\cdot$d$^{-1}$ ($P > 0.10$) throughout the rest of the trial. Once-daily milking did not affect the contents of milk fat, true protein, serum albumin and lactose contents or somatic cell count, plasmin activity and plasminogen-derived activity. That treatment also increased the G1 immunoglobulin concentration ($P$ = 0.02; measured at week 3) and reduced milk lipoprotein lipase activity. Once-daily milking improved the nutritional status at the beginning of lactation (reduced live weight and body condition losses, and increased the computed energy balance) and had no effect on the ration intake. The normal- energy diet produced expected results, in relation to the low-energy diet: a significant increase in intake (1.2 kg DM$\cdot$d$^{-1}$), milk yield (3.1 kg$\cdot$d$^{-1}$), milk protein content (2.0 g$\cdot$kg$^{-1}$), and nutritional indices, in particular. The decrease in milk yield induced by once-daily milking during the first three weeks of lactation was 5.5 kg$\cdot$d$^{-1}$ in the low-energy group and 8.5 kg$\cdot$d$^{-1}$ for the normal energy group (non- significant interaction; $P > 0.10$).

The cysteine-rich proteins (CRPs) are a family of highly conserved LIM (an acronym derived from the three gene products lin-11, isl-1 and mec-3) domain proteins that have been implicated in muscle differentiation. All CRP family members characterized so far have been shown to interact with the filamentous actin cross-linker α-actinin. The region of CRP required for this interaction has previously been broadly mapped to the molecule's N-terminal half. Here we report that the α-actinin-binding region of CRP, which we have mapped by using a combination of blot overlay and Western immunoblot techniques, is confined to an 18-residue sequence occurring within the protein's N-terminal glycine-rich repeat. A site-directed mutagenesis analysis of the binding region has revealed the critical importance of a single lysine residue (lysine 65 in human CRP1). Alterations at this site lead to a 10-fold decrease in α-actinin binding in comparison with wild-type CRP. The critical lysine residue localizes within a short α-helix, raising the possibility that mutagenesis-induced alterations in α-actinin-binding capacity might be attributed to the disruption of a key structural element.

alpha-Actinin is required for the organization and function of the contractile machinery of muscle. In order to understand more precisely the molecular mechanisms by which alpha-actinin might contribute to the formation and maintenance of the contractile apparatus within muscle cells, we performed a screen to identify novel alpha-actinin binding partners present in chicken smooth muscle cells. In this paper, we report the identification, purification, and characterization of a 36-kDa smooth muscle protein (p36) that interacts with alpha-actinin. Using a variety of in vitro binding assays, we demonstrate that the association between alpha-actinin and p36 is direct, specific, and saturable and exhibits a moderate affinity. Furthermore, native co-immunoprecipitation reveals that the two proteins are complexed in vivo. p36 is expressed in cardiac muscle and tissues enriched in smooth muscle. Interestingly, in skeletal muscle, a closely related protein of 40 kDa (p40) is detected. The expression of p36 and p40 is dramatically up-regulated during smooth and skeletal muscle differentiation, respectively, and p40 colocalizes with alpha-actinin at the Z-lines of differentiated myotubes. We have established the relationship between p36 and p40 by molecular cloning of cDNAs that encode both proteins and have determined that they are the products of a single gene. Both proteins display an identical N-terminal PDZ domain and an identical C-terminal LIM domain; an internal 63-amino acid sequence present in p36 is replaced by a unique 111-amino acid sequence in p40. Analysis of the sequences of p36 and p40 suggest that they are the avian forms of the actinin-associated LIM proteins (ALPs) recently described in rat (Xia, H., Winokur, S. T., Kuo, W.-L., Altherr, M. R., and Bredt, D. S. (1997) J. Cell Biol. 139, 507-515). The expression of the human ALP gene has been postulated to be affected by mutations that cause facioscapulohumeral muscular dystrophy; thus, the characterization of ALP function may ultimately provide insight into the mechanism of this disease.

α-Actinin is required for the organization and function of the contractile machinery of muscle. In order to understand more precisely the molecular mechanisms by which α-actinin might contribute to the formation and maintenance of the contractile apparatus within muscle cells, we performed a screen to identify novel α-actinin binding partners present in chicken smooth muscle cells. In this paper, we report the identification, purification, and characterization of a 36-kDa smooth muscle protein (p36) that interacts with α-actinin. Using a variety of in vitrobinding assays, we demonstrate that the association between α-actinin and p36 is direct, specific, and saturable and exhibits a moderate affinity. Furthermore, native co-immunoprecipitation reveals that the two proteins are complexed in vivo. p36 is expressed in cardiac muscle and tissues enriched in smooth muscle. Interestingly, in skeletal muscle, a closely related protein of 40 kDa (p40) is detected. The expression of p36 and p40 is dramatically up-regulated during smooth and skeletal muscle differentiation, respectively, and p40 colocalizes with α-actinin at the Z-lines of differentiated myotubes. We have established the relationship between p36 and p40 by molecular cloning of cDNAs that encode both proteins and have determined that they are the products of a single gene. Both proteins display an identical N-terminal PDZ domain and an identical C-terminal LIM domain; an internal 63-amino acid sequence present in p36 is replaced by a unique 111-amino acid sequence in p40. Analysis of the sequences of p36 and p40 suggest that they are the avian forms of the actinin-associated LIM proteins (ALPs) recently described in rat (Xia, H., Winokur, S. T., Kuo, W.-L., Altherr, M. R., and Bredt, D. S. (1997) J. Cell Biol.139, 507–515). The expression of the human ALPgene has been postulated to be affected by mutations that cause facioscapulohumeral muscular dystrophy; thus, the characterization of ALP function may ultimately provide insight into the mechanism of this disease.

We previously reported that the activation of the M promoter of the human choline acetyltransferase (ChAT) gene by butyrate and trapoxin in transfected CHP126 cells is blocked by PD98059, a specific mitogen-activated protein kinase kinase (MEK) inhibitor (E. Espinos and M. J. Weber, Mol. Brain Res. 56:118–124, 1998). We now report that the transcriptional effects of histone deacetylase inhibitors are mediated by an H7-sensitive serine/threonine protein kinase. Activation of the ChAT promoter by butyrate and trapoxin was blocked by 50 μM H7 in both transient- and stable-transfection assays. Overexpression of p300, a coactivator protein endowed with histone acetyltransferase activity, stimulated the ChAT promoter and had a synergistic effect on butyrate treatment. These effects were blocked by H7 and by overexpressed adenovirus E1A 12S protein. Moreover, both H7 and PD98059 suppressed the activation of the Rous sarcoma virus (RSV) and simian virus 40 promoters by butyrate in transfection experiments. Similarly, the induction of the cellular histone H10gene by butyrate in CHP126 cells was blocked by H7 and by PD98059. Previous data (L. Cuisset, L. Tichonicky, P. Jaffray, and M. Delpech, J. Biol. Chem. 272:24148–24153, 1997) showed that the induction of the H10gene by butyrate is blocked by okadaic acid, an inhibitor of protein phosphatases. We now show that the activation of the ChAT and RSV promoters by butyrate in transfected CHP126 cells is also blocked by 200 nM okadaic acid. Western blotting and in vivo metabolic labeling experiments showed that butyrate has a biphasic effect on histone H3 phosphorylation, i.e., depression for up to 16 h followed by stimulation. The data thus strongly suggest that the transcriptional effects of histone deacetylase inhibitors are mediated through the activation of MEK1 and of an H7-sensitive protein kinase in addition to protein phosphatases.

Members of the cysteine-rich protein (CRP) family are evolutionarily conserved proteins that have been implicated in the processes of cell proliferation and differentiation. In particular, one CRP family member has been shown to be an essential regulator of cardiac and skeletal muscle development. Each of the three vertebrate CRP isoforms characterized to date is composed of two copies of the zinc-binding LIM domain with associated glycine-rich repeats. In this study, we have addressed the biological significance of the CRP multigene family by comparing the subcellular distributions, biochemical properties, and expression patterns of CRP1, CRP2, and CRP3/MLP. Our data reveal that all three CRP family members, when expressed in adherent fibroblasts, associate specifically with the actin cytoskeleton. Moreover, all three CRP isoforms are capable of interacting with the cytoskeletal proteins alpha-actinin and zyxin. Together, these observations suggest that CRP family members may exhibit overlapping cellular functions. Differences between the three CRPs are evident in their protein expression patterns in chick embryos. CRP1 expression is detected in a variety of organs enriched in smooth muscle. CRP2 is restricted to arteries and fibroblasts. CRP3/MLP is dominant in organs enriched in striated muscle. CRP isoform expression is also developmentally regulated in the chick. Our findings suggest that the three CRP family members perform similar functions in different muscle derivatives. The demonstration that all members of the CRP family are associated with cytoskeletal components that have been implicated in the assembly and organization of filamentous actin suggests that CRPs contribute to muscle cell differentiation via effects on cytoarchitecture.

This article describes how RNA expression data of 173 genes were produced on 384 sunflower hybrids grown in field conditions. Sunflower hybrids were selected to represent genetic diversity within cultivated sunflower. The RNA was extracted from mature leaves at one time seven days after anthesis. These data allow to differentiate the different genotype behaviours and constitute a valuable resource to the community to study the adaptation of crops to field conditions and the molecular basis of heterosis. It is available on data.inra.fr repository.

This article describes how the transcriptomic data were produced on sunflower plants subjected to water deficit. Twenty-four sunflower (Helianthus annuus) genotypes were selected to represent genetic diversity within cultivated sunflower and included both inbred lines and their hybrids. Drought stress was applied to plants in pots at the vegetative stage using the high-throughput phenotyping platform Heliaphen. Here, we provide transcriptomic data from sunflower leaves. These data differentiate both plant water status and the different genotypes. They constitute a valuable resource to the community to study adaptation of crops to drought and the transcriptomic basis of heterosis.

Recent research studies have explored what digital platforms do as well as the behaviour they generate among users. This article builds on the existing literature by studying how P2P digital platforms are speeding up market activities and how this acceleration is shaping inter-user relationships. A qualitative ethnographic study was conducted on the secondhand clothing market from 2013 to 2020. Drawing on social acceleration theory, we show how the affordances of digital platforms encourage an acceleration in the pace of life, an acceleration in the renewal of items owned, and a technical acceleration across multiple domains. These accelerations are inciting speed-based competition between users, who must now be more responsive, more trend-conscious, and more savvy than others. The platforms also constitute a particular digital space that invites us to rethink the notion of alienation in various forms, specifically spatial and temporal alienation. In addition to these theoretical contributions, this research offers societal insights that will help users become more aware of the scale of their sped-up activities on digital platforms.