scholarly journals Neuro-molecular characterization of fish cleaning interactions

2021 ◽  
Author(s):  
Sandra Ramirez-Calero ◽  
Jose Ricardo Paula ◽  
Eve Otjacques ◽  
Rui Rosa ◽  
Timothy Ravasi ◽  
...  
Keyword(s):  
Cognitive Abilities ◽  
Molecular Mechanisms ◽  
Interspecific Interactions ◽  
Transcriptional Response ◽  
Early Gene ◽  
Pituitary Hormone ◽  
Molecular Alterations ◽  
Hormone Responses ◽  
Social Decision Making ◽  
Glutamatergic Pathways

Coral reef fish exhibit a large variety of behaviours crucial for fitness and survival. The cleaner wrasse Labroides dimidiatus displays cognitive abilities during interspecific interactions by providing services of ectoparasite cleaning, thus serving as a good model to understand the processes of complex social behaviour. However, little is known about the molecular underpinnings of cooperative behaviour between L. dimidiatus and a potential client fish (Acanthurus leucosternon). Therefore, we investigated the molecular mechanisms in three regions of the brain (fore-, mid-, and hindbrain) during the interaction of these fishes. Here we show, using transcriptomics, that most of the transcriptional response in both species was regulated in the hindbrain and forebrain regions and that the interacting behaviour responses of L. dimidiatus involved immediate early gene alteration, dopaminergic and glutamatergic pathways, the expression of neurohormones (such as isotocin) and steroids (e.g. progesterone and estrogen), as well as social decision-making genes. In contrast, in the client, fewer molecular alterations were found, mostly involving pituitary hormone responses. The particular pathways found suggested learning and memory processes in the cleaner wrasse, while the client indicated stress relief and a reduction in aggression.

scholarly journals Blunted transcriptional response to skeletal muscle ischemia in rats with chronic kidney disease: potential role for impaired ischemia-induced angiogenesis

2017 ◽  
Vol 49 (4) ◽  
pp. 230-237 ◽  
Author(s):  
Rafael U. Heiss ◽  
Fabian B. Fahlbusch ◽  
Johannes Jacobi ◽  
Christoph Daniel ◽  
Arif B. Ekici ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Differentially Expressed ◽  
Early Gene ◽  
Male Rats ◽  
Pcr Analysis ◽  
Cardiovascular Morbidity And Mortality

Chronic kidney disease (CKD) is associated with increased cardiovascular morbidity and mortality. Previous studies indicated an impairment of ischemia-induced angiogenesis in skeletal muscle of rats with CKD. We performed a systematic comparison of early gene expression in response to ischemia in rats with or without CKD to identify potential molecular mechanisms underlying impaired angiogenesis in CKD. CKD was induced in male rats by 5/6 nephrectomy (SNX); control rats were sham operated (sham). Eight weeks later, ischemia of the right limb was induced by ligation and resection of the femoral artery. Rats were killed 24 h after the onset of ischemia, and RNA was extracted from the musculus soleus of the ischemic and the nonischemic hindlimb. To identify differentially expressed transcripts, we analyzed RNA with Affymetrix GeneChip Rat Genome 230 2.0 Arrays. RT-PCR analysis of selected genes was performed to validate observed changes. Hindlimb ischemia upregulated 239 genes in CKD and 299 genes in control rats (66% overlap), whereas only a few genes were downregulated (14 in CKD and 34 in controls) compared with the nonischemic limb of the same animals. Comparison between the ischemic limbs of CKD and controls revealed downregulation of 65 genes in CKD; 37 of these genes were also among the ischemia-induced genes in controls. Analysis of functional groups (other than angiogenesis) pointed to genes involved in leukocyte recruitment and fatty acid metabolism. Transcript expression profiling points to a relatively small number of differentially expressed genes that may underlie the impaired postischemic angiogenesis in CKD.

scholarly journals Examination of the Transcriptional Response to LaMIR166a Overexpression in Larix kaempferi (Lamb.) Carr

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 576
Author(s):  
Yanru Fan ◽  
Wanfeng Li ◽  
Zhexin Li ◽  
Shaofei Dang ◽  
Suying Han ◽  
...  
Keyword(s):  
Cell Lines ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
De Novo ◽  
Pearson Correlation ◽  
Transcriptional Response ◽  
Correlation Coefficients ◽  
Embryonic Cell ◽  
Larix Kaempferi ◽  
Transgenic Cell

The study of somatic embryogenesis can provide insight into early plant development. We previously obtained LaMIR166a-overexpressing embryonic cell lines of Larix kaempferi (Lamb.) Carr. To further elucidate the molecular mechanisms associated with miR166 in this species, the transcriptional profiles of wild-type (WT) and three LaMIR166a-overexpressing transgenic cell lines were subjected to RNA sequencing using the Illumina NovaSeq 6000 system. In total, 203,256 unigenes were generated using Trinity de novo assembly, and 2467 differentially expressed genes were obtained by comparing transgenic and WT lines. In addition, we analyzed the cleaved degree of LaMIR166a target genes LaHDZ31–34 in different transgenic cell lines by detecting the expression pattern of LaHdZ31–34, and their cleaved degree in transgenic cell lines was higher than that in WT. The downstream genes of LaHDZ31–34 were identified using Pearson correlation coefficients. Yeast one-hybrid and dual-luciferase report assays revealed that the transcription factors LaHDZ31–34 could bind to the promoters of LaPAP, LaPP1, LaZFP5, and LaPHO1. This is the first report of gene expression changes caused by LaMIR166a overexpression in Japanese larch. These findings lay a foundation for future studies on the regulatory mechanism of miR166.

scholarly journals Wedding of Molecular Alterations and Immune Checkpoint Blockade: Genomics as a Matchmaker

2021 ◽  
Author(s):  
Elena Fountzilas ◽  
Razelle Kurzrock ◽  
Henry Hiep Vo ◽  
Apostolia-Maria Tsimberidou
Keyword(s):  
Molecular Mechanisms ◽  
Cell Receptor ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
Beta Catenin ◽  
Molecular Alterations ◽  
Receptor Repertoire ◽  
Repair Deficiency ◽  
Tumor Mutational Burden

Abstract The development of checkpoint blockade immunotherapy has transformed the medical oncology armamentarium. But, despite its favorable impact on clinical outcomes, immunotherapy benefits only a subset of patients, and a substantial proportion of these individuals eventually manifest resistance. Serious immune-related adverse events and hyper-progression have also been reported. It is therefore essential to understand the molecular mechanisms and identify the drivers of therapeutic response and resistance. In this review, we provide an overview of the current and emerging clinically relevant genomic biomarkers implicated in checkpoint blockade outcome. U.S. Food and Drug Administration–approved molecular biomarkers of immunotherapy response include mismatch repair deficiency/microsatellite instability and tumor mutational burden ≥10 mutations/megabase. Investigational genomic-associated biomarkers for immunotherapy response include alterations of the following genes/associated pathways: chromatin remodeling (ARID1A, PBRM1, SMARCA4, SMARCB1, BAP1), major histocompatibility complex, specific (e.g., ultraviolet, APOBEC) mutational signatures, T-cell receptor repertoire, PDL1, POLE/POLD1, and neo-antigens produced by the mutanome; those potentially associated with resistance include β2-microglobulin, EGFR, Keap1, JAK1/JAK2/interferon-gamma signaling, MDM2, PTEN, STK11, and Wnt/Beta-catenin pathway alterations. Prospective clinical trials are needed to assess the role of a composite of these biomarkers in order to optimize the implementation of precision immunotherapy in patient care.

scholarly journals Molecular Alterations in Sporadic and SOD1-ALS Immortalized Lymphocytes: Towards a Personalized Therapy

2021 ◽  
Vol 22 (6) ◽  
pp. 3007
Author(s):  
Isabel Lastres-Becker ◽  
Gracia Porras ◽  
Marina Arribas-Blázquez ◽  
Inés Maestro ◽  
Daniel Borrego-Hernández ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Therapeutic Interventions ◽  
Autophagic Flux ◽  
Metabolic Disturbances ◽  
Molecular Alterations ◽  
Healthy Donors ◽  
Inflammatory Profile ◽  
Als Patients

Amyotrophic lateral sclerosis (ALS) is a fatal neurological condition where motor neurons (MNs) degenerate. Most of the ALS cases are sporadic (sALS), whereas 10% are hereditarily transmitted (fALS), among which mutations are found in the gene that codes for the enzyme superoxide dismutase 1 (SOD1). A central question in ALS field is whether causative mutations display selective alterations not found in sALS patients, or they converge on shared molecular pathways. To identify specific and common mechanisms for designing appropriate therapeutic interventions, we focused on the SOD1-mutated (SOD1-ALS) versus sALS patients. Since ALS pathology involves different cell types other than MNs, we generated lymphoblastoid cell lines (LCLs) from sALS and SOD1-ALS patients and healthy donors and investigated whether they show changes in oxidative stress, mitochondrial dysfunction, metabolic disturbances, the antioxidant NRF2 pathway, inflammatory profile, and autophagic flux. Both oxidative phosphorylation and glycolysis appear to be upregulated in lymphoblasts from sALS and SOD1-ALS. Our results indicate significant differences in NRF2/ARE pathway between sALS and SOD1-ALS lymphoblasts. Furthermore, levels of inflammatory cytokines and autophagic flux discriminate between sALS and SOD1-ALS lymphoblasts. Overall, different molecular mechanisms are involved in sALS and SOD1-ALS patients and thus, personalized medicine should be developed for each case.

scholarly journals Onco-Multi-OMICS Approach: A New Frontier in Cancer Research

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Sajib Chakraborty ◽  
Md. Ismail Hosen ◽  
Musaddeque Ahmed ◽  
Hossain Uddin Shekhar
Keyword(s):  
Cancer Research ◽  
Systems Biology ◽  
Cancer Cells ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
The Cancer Genome Atlas ◽  
Resolving Power ◽  
Cancer Hallmarks ◽  
Molecular Alterations ◽  
Integrated Omics

The acquisition of cancer hallmarks requires molecular alterations at multiple levels including genome, epigenome, transcriptome, proteome, and metabolome. In the past decade, numerous attempts have been made to untangle the molecular mechanisms of carcinogenesis involving single OMICS approaches such as scanning the genome for cancer-specific mutations and identifying altered epigenetic-landscapes within cancer cells or by exploring the differential expression of mRNA and protein through transcriptomics and proteomics techniques, respectively. While these single-level OMICS approaches have contributed towards the identification of cancer-specific mutations, epigenetic alterations, and molecular subtyping of tumors based on gene/protein-expression, they lack the resolving-power to establish the casual relationship between molecular signatures and the phenotypic manifestation of cancer hallmarks. In contrast, the multi-OMICS approaches involving the interrogation of the cancer cells/tissues in multiple dimensions have the potential to uncover the intricate molecular mechanism underlying different phenotypic manifestations of cancer hallmarks such as metastasis and angiogenesis. Moreover, multi-OMICS approaches can be used to dissect the cellular response to chemo- or immunotherapy as well as discover molecular candidates with diagnostic/prognostic value. In this review, we focused on the applications of different multi-OMICS approaches in the field of cancer research and discussed how these approaches are shaping the field of personalized oncomedicine. We have highlighted pioneering studies from “The Cancer Genome Atlas (TCGA)” consortium encompassing integrated OMICS analysis of over 11,000 tumors from 33 most prevalent forms of cancer. Accumulation of huge cancer-specific multi-OMICS data in repositories like TCGA provides a unique opportunity for the systems biology approach to tackle the complexity of cancer cells through the unification of experimental data and computational/mathematical models. In future, systems biology based approach is likely to predict the phenotypic changes of cancer cells upon chemo-/immunotherapy treatment. This review is sought to encourage investigators to bring these different approaches together for interrogating cancer at molecular, cellular, and systems levels.

fra-1: a serum-inducible, cellular immediate-early gene that encodes a fos-related antigen

1988 ◽  
Vol 8 (5) ◽  
pp. 2063-2069 ◽  
Author(s):  
D R Cohen ◽  
T Curran
Keyword(s):  
Regulatory Protein ◽  
Transcriptional Response ◽  
Early Gene ◽  
Immediate Early ◽  
Cdna Clones ◽  
Protein Synthesis Inhibitors ◽  
Amino Acid Homology ◽  
Serum Stimulation ◽  
Fos Protein ◽  
Genes Encoding

A set of proteins antigenically related to the c-fos protein (Fos) are induced by serum in fibroblasts. To isolate cDNA clones of genes encoding such proteins, a lambda gt11 expression cDNA library constructed from serum-stimulated rat fibroblasts was screened with antibodies raised against a hydrophilic region (amino acids 127 to 152) of Fos. One of the positive clones identified, termed fra-1 (Fos-related antigen) was characterized. It encoded a protein that shared several regions of extensive amino acid homology with Fos (including the region that showed similarity to both the yeast GCN4 regulatory protein and the protein encoded by the jun oncogene), although its nucleotide sequence was considerably diverged from that of the c-fos gene. Only a subset of the agents and conditions that activated c-fos also induced fra-1. Induction of fra-1 expression following serum stimulation was delayed compared with that of c-fos. However, like c-fos, fra-1 was induced rapidly by serum in the presence of protein synthesis inhibitors. Thus, a family of Fos-related, inducible genes are involved in the cellular immediate-early transcriptional response to extracellular stimuli.

scholarly journals ‘Candidatus Phytoplasma solani’ interferes with the distribution and uptake of iron in tomato

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Sara Buoso ◽  
Laura Pagliari ◽  
Rita Musetti ◽  
Marta Martini ◽  
Fabio Marroni ◽  
...  
Keyword(s):  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Transcriptome Profiling ◽  
Transport Processes ◽  
Fe Deficiency ◽  
Cultivated Plants ◽  
Chlorophyll Metabolism ◽  
Wide Range ◽  
Phytoplasma Infection

Abstract Background ‘Candidatus Phytoplasma solani’ is endemic in Europe and infects a wide range of weeds and cultivated plants. Phytoplasmas are prokaryotic plant pathogens that colonize the sieve elements of their host plant, causing severe alterations in phloem function and impairment of assimilate translocation. Typical symptoms of infected plants include yellowing of leaves or shoots, leaf curling, and general stunting, but the molecular mechanisms underlying most of the reported changes remain largely enigmatic. To infer a possible involvement of Fe in the host-phytoplasma interaction, we investigated the effects of ‘Candidatus Phytoplasma solani’ infection on tomato plants (Solanum lycopersicum cv. Micro-Tom) grown under different Fe regimes. Results Both phytoplasma infection and Fe starvation led to the development of chlorotic leaves and altered thylakoid organization. In infected plants, Fe accumulated in phloem tissue, altering the local distribution of Fe. In infected plants, Fe starvation had additive effects on chlorophyll content and leaf chlorosis, suggesting that the two conditions affected the phenotypic readout via separate routes. To gain insights into the transcriptional response to phytoplasma infection, or Fe deficiency, transcriptome profiling was performed on midrib-enriched leaves. RNA-seq analysis revealed that both stress conditions altered the expression of a large (> 800) subset of common genes involved in photosynthetic light reactions, porphyrin / chlorophyll metabolism, and in flowering control. In Fe-deficient plants, phytoplasma infection perturbed the Fe deficiency response in roots, possibly by interference with the synthesis or transport of a promotive signal transmitted from the leaves to the roots. Conclusions ‘Candidatus Phytoplasma solani’ infection changes the Fe distribution in tomato leaves, affects the photosynthetic machinery and perturbs the orchestration of root-mediated transport processes by compromising shoot-to-root communication.

scholarly journals Molecular Alterations in Sporadic Primary Hyperparathyroidism

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Inês Alvelos ◽  
Maria Mendes ◽  
Paula Soares
Keyword(s):  
Primary Hyperparathyroidism ◽  
Molecular Mechanisms ◽  
Benign Lesion ◽  
Protein Overexpression ◽  
Endocrine Disorder ◽  
Molecular Alterations ◽  
Familial Form ◽  
Somatic Alterations ◽  
Sporadic Primary Hyperparathyroidism ◽  
Parathyroid Tumours

Primary hyperparathyroidism (PHPT) is a frequent endocrine disorder characterized by an excessive autonomous production and release of parathyroid hormone (PTH) by the parathyroid glands. This endocrinopathy may result from the development of a benign lesion (adenoma or hyperplasia) or from a carcinoma. Most of the PHPT cases occur sporadically; however, approximately 10% of the patients present a familial form of the disease. The molecular mechanisms underlying the pathogenesis of sporadic PHPT are incompletely understood, even though somatic alterations in MEN1 gene and CCND1 protein overexpression are frequently observed. The MEN1 gene is mutated in about 30% of the parathyroid tumours and the protooncogene CCND1 is implicated in parathyroid neoplasia by rearrangements, leading to an overexpression of CCND1 protein in parathyroid cells. The aim of this work is to briefly update the molecular alterations underlying sporadic primary hyperparathyroidism.

scholarly journals Forebrain Transcriptional Response to Transient Changes in Circulating Androgens in a Cichlid Fish

2020 ◽  
Vol 10 (6) ◽  
pp. 1971-1982
Author(s):  
Ana S. Félix ◽  
Sara D. Cardoso ◽  
António Roleira ◽  
Rui F. Oliveira
Keyword(s):  
Cichlid Fish ◽  
Behavioral Flexibility ◽  
Transcriptional Response ◽  
Brain Network ◽  
Behavioral Changes ◽  
Membrane Receptors ◽  
Control Fish ◽  
The Social ◽  
Social Decision Making ◽  
Androgen Levels

It has been hypothesized that androgens respond to the social interactions as a way to adjust the behavior of individuals to the challenges of the social environment in an adaptive manner. Therefore, it is expected that transient changes in circulating androgen levels within physiological scope should impact the state of the brain network that regulates social behavior, which should translate into adaptive behavioral changes. Here, we examined the effect that a transient peak in androgen circulating levels, which mimics socially driven changes in androgen levels, has on the forebrain state, which harbors most nuclei of the social decision-making network. For this purpose, we successfully induced transient changes in circulating androgen levels in an African cichlid fish (Mozambique tilapia, Oreochromis mossambicus) commonly used as a model in behavioral neuroendocrinology by injecting 11-ketotestosterone or testosterone, and compared the forebrain transcriptome of these individuals to control fish injected with vehicle. Forebrain samples were collected 30 min and 60 min after injection and analyzed using RNAseq. Our results showed that a transient peak in 11-ketotestosterone drives more accentuated changes in forebrain transcriptome than testosterone, and that transcriptomic impact was greater at the 30 min than at the 60 min post-androgen administration. Several genes involved in the regulation of translation, steroid metabolism, ion channel membrane receptors, and genes involved in epigenetic mechanisms were differentially expressed after 11-ketotestosterone or testosterone injection. In summary, this study identified specific candidate genes that may regulate socially driven changes in behavioral flexibility mediated by androgens.

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