scholarly journals RNA-Seq analysis of isolated satellite cells in Prmt5 deficient mice

Genomics Data ◽  
2015 ◽  
Vol 5 ◽  
pp. 122-125 ◽  
Author(s):  
Carsten Kuenne ◽  
Stefan Guenther ◽  
Mario Looso ◽  
Ting Zhang ◽  
Marcus Krueger ◽  
...  
Keyword(s):  
Satellite Cells ◽  
Rna Seq ◽  
Deficient Mice

scholarly journals Satellite Cell Depletion Disrupts Transcriptional Coordination and Muscle Adaptation to Exercise

Function ◽  
2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Davis A Englund ◽  
Vandré C Figueiredo ◽  
Cory M Dungan ◽  
Kevin A Murach ◽  
Bailey D Peck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Gene Networks ◽  
Wheel Running ◽  
Skeletal Muscle Regeneration ◽  
Rna Seq ◽  
Muscle Adaptation ◽  
Hypertrophic Growth ◽  
Adaptation To Exercise

Abstract Satellite cells are required for postnatal development, skeletal muscle regeneration across the lifespan, and skeletal muscle hypertrophy prior to maturity. Our group has aimed to address whether satellite cells are required for hypertrophic growth in mature skeletal muscle. Here, we generated a comprehensive characterization and transcriptome-wide profiling of skeletal muscle during adaptation to exercise in the presence or absence of satellite cells in order to identify distinct phenotypes and gene networks influenced by satellite cell content. We administered vehicle or tamoxifen to adult Pax7-DTA mice and subjected them to progressive weighted wheel running (PoWeR). We then performed immunohistochemical analysis and whole-muscle RNA-seq of vehicle (SC+) and tamoxifen-treated (SC−) mice. Further, we performed single myonuclear RNA-seq to provide detailed information on how satellite cell fusion affects myonuclear transcription. We show that while skeletal muscle can mount a robust hypertrophic response to PoWeR in the absence of satellite cells, growth, and adaptation are ultimately blunted. Transcriptional profiling reveals several gene networks key to muscle adaptation are altered in the absence of satellite cells.

scholarly journals The gastrointestinal development ‘parts list’: transcript profiling of embryonic gut development in wildtype and Ret-deficient mice

2019 ◽  
Author(s):  
Sumantra Chatterjee ◽  
Priyanka Nandakumar ◽  
Dallas R. Auer ◽  
Stacey B. Gabriel ◽  
Aravinda Chakravarti
Keyword(s):  
Hirschsprung Disease ◽  
Major Effect ◽  
Enteric Neurons ◽  
Null Mouse ◽  
Wildtype Mouse ◽  
Rna Seq ◽  
Gut Development ◽  
Molecular Processes ◽  
The Universe ◽  
Deficient Mice

AbstractThe development of the gut from endodermal tissue to an organ with multiple distinct structures and functions occurs over a prolonged time during embryonic days E10.5-E14.5 in the mouse. During this process, one major event is innervation of the gut by enteric neural crest cells (ENCC) to establish the enteric nervous system (ENS). To understand the molecular processes underpinning gut and ENS development, we generated RNA-seq profiles from wildtype mouse guts at E10.5, E12.5 and E14.5 from both sexes. We also generated these profiles from homozygous Ret null embryos, a model for Hirschsprung disease (HSCR), in whom the ENS is absent. These data reveal four major features: (1) between E10.5 to E14.5 the developmental genetic programs change from expression of major transcription factors (TF) and its modifiers to genes controlling tissue (epithelium, muscle, endothelium) specialization; (2) the major effect of Ret is not only on ENCC differentiation to enteric neurons but also on the enteric mesenchyme and epithelium; (3) a muscle genetic program exerts significant effects on ENS development, and (4) sex differences in gut development profiles are minor. The genetic programs identified, and their changes across development, suggests that both cell autonomous and non-autonomous factors, and interactions between the different developing gut tissues, are important for normal ENS development and its disorders.Significance statementThe mammalian gut is a complex set of tissues formed during development by orchestrating the timing of expression of many genes. Here we uncover the identity of these genes, their pathways and how they change during gut organogenesis. We used RNA-seq profiling in the wildtype mouse gut in both sexes during development (E10.5 - E14.5), as well as in a Ret null mouse, a model of Hirschsprung disease (HSCR). These studies have allowed us to expand the universe of genes and developmental processes that contribute to enteric neuronal innervation and to its dysregulation in disease.

scholarly journals RNASeq analysis of a Pax3-expressing myoblast clone in-vitro and effect of culture surface stiffness on differentiation.

2021 ◽  
Author(s):  
Louise Richardson ◽  
Dapeng Wang ◽  
Ruth E Hughes ◽  
Colin Anfimov Johnson ◽  
Michelle Peckham
Keyword(s):  
Gene Expression ◽  
Satellite Cells ◽  
Cell Clone ◽  
Rna Seq ◽  
Myogenic Regulatory Factors ◽  
Culture Surface ◽  
Γ Interferon ◽  
Cells Cultured ◽  
Sarcomeric Genes

Skeletal muscle satellite cells cultured on soft surfaces (12kPa) show improved differentiation than cells cultured on stiff surfaces (approximately 100kPa). To better understand the reasons for this, we performed an RNA Seq analysis for a single satellite cell clone (C1F) derived from the H2kb-tsA58 immortomouse, which differentiates into myotubes under tightly regulated conditions (withdrawal of γ-interferon, 37°C). As expected, the largest change in overall gene expression occurred at day 1, as cells switch from proliferation to differentiation. Surprisingly, further analysis showed that proliferating C1F cells express Pax3 and not Pax7, confirmed by immunostaining, yet their subsequent differentiation into myotubes is normal, and enhanced on softer surfaces, as evidenced by significantly higher expression levels of myogenic regulatory factors, sarcomeric genes, enhanced fusion and improved myofibrillogenesis. Levels of RNA encoding extracellular matrix structural constituents and related genes were consistently upregulated on hard surfaces, suggesting that a consequence of differentiating satellite cells on hard surfaces is that they attempt to manipulate their niche prior to differentiating. This comprehensive RNASeq dataset will be a useful resource for understanding Pax3 expressing cells.

scholarly journals Cx3cr1-deficient microglia exhibit a premature aging transcriptome

2019 ◽  
Vol 2 (6) ◽  
pp. e201900453 ◽  
Author(s):  
Stefka Gyoneva ◽  
Raghavendra Hosur ◽  
David Gosselin ◽  
Baohong Zhang ◽  
Zhengyu Ouyang ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Immunohistochemical Analysis ◽  
Premature Aging ◽  
Rna Seq ◽  
Active Chromatin ◽  
Chronological Aging ◽  
Transcriptomic Signature ◽  
Immune Related Genes ◽  
Old Mice ◽  
Deficient Mice

CX3CR1, one of the highest expressed genes in microglia in mice and humans, is implicated in numerous microglial functions. However, the molecular mechanisms underlying Cx3cr1 signaling are not well understood. Here, we analyzed transcriptomes of Cx3cr1-deficient microglia under varying conditions by RNA-sequencing (RNA-seq). In 2-mo-old mice, Cx3cr1 deletion resulted in the down-regulation of a subset of immune-related genes, without substantial epigenetic changes in markers of active chromatin. Surprisingly, Cx3cr1-deficient microglia from young mice exhibited a transcriptome consistent with that of aged Cx3cr1-sufficient animals, suggesting a premature aging transcriptomic signature. Immunohistochemical analysis of microglia in young and aged mice revealed that loss of Cx3cr1 modulates microglial morphology in a comparable fashion. Our results suggest that CX3CR1 may regulate microglial function in part by modulating the expression levels of a subset of inflammatory genes during chronological aging, making Cx3cr1-deficient mice useful for studying aged microglia.

scholarly journals Atoh7-independent specification of retinal ganglion cell identity

2020 ◽  
Author(s):  
Justin Brodie-Kommit ◽  
Brian S. Clark ◽  
Qing Shi ◽  
Fion Shiau ◽  
Dong Won Kim ◽  
...  
Keyword(s):  
Visual Information ◽  
Ganglion Cells ◽  
Axonal Guidance ◽  
Retinal Ganglion ◽  
Rna Seq ◽  
Loss Of Function ◽  
Retinal Circuitry ◽  
The Brain ◽  
Deficient Mice ◽  
Modest Reduction

AbstractRetinal ganglion cells (RGCs), which relay visual information from the eye to the brain, are the first cell type generated during retinal neurogenesis. Loss of function of the transcription factor Atoh7, which is expressed in multipotent early neurogenic retinal progenitor cells, leads to a selective and near complete loss of RGCs. Atoh7 has thus been considered essential for conferring competence on progenitors to generate RGCs. However, when apoptosis is inhibited in Atoh7-deficient mice by loss of function of Bax, only a modest reduction in RGC number is observed. Single-cell RNA-Seq of Atoh7;Bax-deficient retinas shows that RGC differentiation is delayed, but that RGC precursors are grossly normal. Atoh7;Bax-deficient RGCs eventually mature, fire action potentials, and incorporate into retinal circuitry, but exhibit severe axonal guidance defects. This study reveals an essential role for Atoh7 in RGC survival, and demonstrates Atoh7-independent mechanisms for RGC specification.

scholarly journals G6pd-Deficient Mice Are Protected From Experimental Cerebral Malaria and Liver Injury by Suppressing Proinflammatory Response in the Early Stage of Plasmodium berghei Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Haoan Yi ◽  
Weiyang Jiang ◽  
Fang Yang ◽  
Fan Li ◽  
Yirong Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
G6pd Deficiency ◽  
Acute Liver Injury ◽  
Underlying Mechanism ◽  
Rna Seq ◽  
Proinflammatory Response ◽  
Experimental Cerebral Malaria ◽  
Proinflammatory Responses ◽  
Deficient Mice

Epidemiological studies provide compelling evidence that glucose-6-phosphate dehydrogenase (G6PD) deficiency individuals are relatively protected against Plasmodium parasite infection. However, the animal model studies on this subject are lacking. Plus, the underlying mechanism in vivo is poorly known. In this study, we used a G6pd-deficient mice infected with the rodent parasite Plasmodium berghei (P.berghei) to set up a malaria model in mice. We analyzed the pathological progression of experimental cerebral malaria (ECM) and acute liver injury in mice with different G6pd activity infected with P.berghei. We performed dual RNA-seq for host-parasite transcriptomics and validated the changes of proinflammatory response in the murine model. G6pd-deficient mice exhibited a survival advantage, less severe ECM and mild liver injury compared to the wild type mice. Analysis based on dual RNA-seq suggests that G6pd-deficient mice are protected from ECM and acute liver injury were related to proinflammatory responses. Th1 differentiation and dendritic cell maturation in the liver and spleen were inhibited in G6pd-deficient mice. The levels of proinflammatory cytokines were reduced, chemokines and vascular adhesion molecules in the brain were significantly down-regulated, these led to decreased cerebral microvascular obstruction in G6pd-deficient mice. We generated the result that G6pd-deficiency mediated protection against ECM and acute liver injury were driven by the regulatory proinflammatory responses. Furthermore, bioinformatics analyses showed that P.berghei might occur ribosome loss in G6pd-deficient mice. Our findings provide a novel perspective of the underlying mechanism of G6PD deficiency mediated protection against malaria in vivo.

Activin A Determines Steroid Levels and Composition in the Fetal Testis

Endocrinology ◽  
2020 ◽  
Vol 161 (7) ◽  
Author(s):  
Penny A F Whiley ◽  
Liza O’Donnell ◽  
Sarah C Moody ◽  
David J Handelsman ◽  
Julia C Young ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Sertoli Cells ◽  
Activin A ◽  
Rna Seq ◽  
Testis Development ◽  
Fetal Testis ◽  
Cell Transcriptome ◽  
First Time ◽  
Dose Dependent ◽  
Deficient Mice

Abstract Activin A promotes fetal mouse testis development, including driving Sertoli cell proliferation and cord morphogenesis, but its mechanisms of action are undefined. We performed ribonucleic acid sequencing (RNA-seq) on testicular somatic cells from fetal activin A-deficient mice (Inhba KO) and wildtype littermates at embryonic day (E) E13.5 and E15.5. Analysis of whole gonads provided validation, and cultures with a pathway inhibitor discerned acute from chronic effects of altered activin A bioactivity. Activin A deficiency predominantly affects the Sertoli cell transcriptome. New candidate targets include Minar1, Sel1l3, Vnn1, Sfrp4, Masp1, Nell1, Tthy1 and Prss12. Importantly, the testosterone (T) biosynthetic enzymes present in fetal Sertoli cells, Hsd17b1 and Hsd17b3, were identified as activin-responsive. Activin-deficient testes contained elevated androstenedione (A4), displayed an Inhba gene dose-dependent A4/T ratio, and contained 11-keto androgens. The remarkable accumulation of lipid droplets in both Sertoli and germ cells at E15.5 indicated impaired lipid metabolism in the absence of activin A. This demonstrated for the first time that activin A acts on Sertoli cells to determine local steroid production during fetal testis development. These outcomes reveal how compounds that perturb fetal steroidogenesis can function through cell-specific mechanisms and can indicate how altered activin levels in utero may impact testis development.

scholarly journals Satellite Cells Exhibit Decreased Numbers and Impaired Functions on Single Myofibers Isolated from Vitamin B6-Deficient Mice

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4531
Author(s):  
Takumi Komaru ◽  
Noriyuki Yanaka ◽  
Thanutchaporn Kumrungsee
Keyword(s):  
Satellite Cells ◽  
Vitamin B6 ◽  
Potential Role ◽  
Cellular Level ◽  
Free Medium ◽  
Self Renewal ◽  
Cell Pool ◽  
Vitamin B6 Deficiency ◽  
And Function ◽  
Deficient Mice

Emerging research in human studies suggests an association among vitamin B6, sarcopenia, and muscle strength. However, very little is known regarding its potential role at the cellular level, especially in muscle satellite cells. Therefore, to determine whether vitamin B6 affects the satellite cells, we isolated single myofibers from muscles of vitamin B6-deficient and vitamin B6-supplemented mice. Subsequently, we subjected them to single myofiber culture and observed the number and function of the satellite cells, which remained in their niche on the myofibers. Prior to culture, the vitamin B6-deficient myofibers exhibited a significantly lower number of quiescent satellite cells, as compared to that in the vitamin B6-supplemented myofibers, thereby suggesting that vitamin B6 deficiency induces a decline in the quiescent satellite cell pool in mouse muscles. After 48 and 72 h of culture, the number of proliferating satellite cells per cluster was similar between the vitamin B6-deficient and -supplemented myofibers, but their numbers decreased significantly after culturing the myofibers in vitamin B6-free medium. After 72 h of culture, the number of self-renewing satellite cells per cluster was significantly lower in the vitamin B6-deficient myofibers, and the vitamin B6-free medium further decreased this number. In conclusion, vitamin B6 deficiency appears to reduce the number of quiescent satellite cells and suppress the proliferation and self-renewal of satellite cells during myogenesis.

Comparison of localization of metallothionein in tissues of metallothionein-deficient mice

1995 ◽  
Vol 53 ◽  
pp. 1042-1043
Author(s):  
H. Nishimura ◽  
R Nishimura ◽  
D.L. Adelson ◽  
A.E. Michaelska ◽  
K.H.A. Choo ◽  
...  
Keyword(s):  
Metal Binding ◽  
Immunohistochemical Staining ◽  
Squamous Epithelium ◽  
Rabbit Antiserum ◽  
Slight Modification ◽  
Positive Control ◽  
Heavy Metal Binding ◽  
Critical Organ ◽  
Metal Binding Protein ◽  
Deficient Mice

Metallothionein (MT), a cysteine-rich heavy metal binding protein, has several isoforms designated from I to IV. Its major isoforms, I and II, can be induced by heavy metals like cadmium (Cd) and, are present in various organs of man and animals. Rodent testes are a critical organ to Cd and it is still a controversial matter whether MT exists in the testis although it is clear that MT is not induced by Cd in this tissue. MT-IV mRNA was found to localize within tongue squamous epithelium. Whether MT-III is present mainly glial cells or neurons has become a debatable topic. In the present study, we have utilized MT-I and II gene targeted mice and compared MT localization in various tissues from both MT-deficient mice and C57Black/6J mice (C57BL) which were used as an MT-positive control. For MT immunostaining, we have used rabbit antiserum against rat MT-I known to cross-react with mammalian MT-I and II and human MT-III. Immunohistochemical staining was conducted by the method described in the previous paper with a slight modification after the tissues were fixed in HistoChoice and embedded in paraffin.

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