scholarly journals Timing of gene expression and recruitment in independent origins of CAM in the Agavoideae (Asparagaceae).

2021 ◽  
Author(s):  
Karolina Heyduk ◽  
Edward McAssey ◽  
James Leebens-Mack
Keyword(s):  
Gene Expression ◽  
Carbon Fixation ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptional Response ◽  
Time Of Day ◽  
Temporal Separation ◽  
Genes Encoding ◽  
Cam Species ◽  
Cam Photosynthesis

CAM photosynthesis has evolved repeatedly across the plant tree of life, yet our understanding of the genetic convergence across independent origins remains hampered by the lack of comparative studies. CAM is furthermore thought to be closely linked to the circadian clock in order to achieve temporal separation of carboxylation and sugar production. Here, we explore gene expression profiles in eight species from the Agavoideae (Asparagaceae) encompassing three independent origins of CAM. Using comparative physiology and transcriptomics, we examined the variable modes of CAM in this subfamily and the changes in gene expression across time of day and between well-watered and drought-stressed treatments. We further assessed gene expression and molecular evolution of genes encoding phosphoenolpyruvate carboxylase (PPC), an enzyme required for primary carbon fixation in CAM. Most time-of-day expression profiles are largely conserved across all eight species and suggest that large perturbations to the central clock are not required for CAM evolution. In contrast, transcriptional response to drought is highly lineage specific. Yucca and Beschorneria have CAM-like expression of PPC2, a copy of PPC that has never been shown to be recruited for CAM in angiosperms, and evidence of positive selection in PPC genes implicates mutations that may have facilitated the recruitment for CAM function early in the evolutionary history of the Agavoideae. Together the physiological and transcriptomic comparison of closely related C3 and CAM species reveals similar gene expression profiles, with the notable exception of differential recruitment of carboxylase enzymes for CAM function.

scholarly journals Glucocorticoid-dependent transcription in skin requires epidermal expression of the glucocorticoid receptor and is modulated by the mineralocorticoid receptor

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Lisa M. Sevilla ◽  
Judit Bigas ◽  
Álvaro Chiner-Oms ◽  
Iñaki Comas ◽  
Vicente Sentandreu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mineralocorticoid Receptor ◽  
Inflammatory Diseases ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptional Response ◽  
Specific Loss ◽  
Relative Contribution ◽  
Effective Use ◽  
Epidermal Expression

Abstract Glucocorticoid (GC) actions are mediated through two closely related ligand-dependent transcription factors, the GC receptor (GR) and the mineralocorticoid receptor (MR). Given the wide and effective use of GCs to combat skin inflammatory diseases, it is important to understand the relative contribution of these receptors to the transcriptional response to topical GCs. We evaluated the gene expression profiles in the skin of mice with epidermal-specific loss of GR (GREKO), MR (MREKO), or both (double KO; DKO) in response to dexamethasone (Dex). The overall transcriptional response was abolished in GREKO and DKO skin suggesting dependence of the underlying dermis on the presence of epidermal GR. Indeed, the observed dermal GC resistance correlated with a constitutive decrease in GR activity and up-regulation of p38 activity in this skin compartment. Upon Dex treatment, more than 90% of differentially expressed genes (DEGs) in CO overlapped with MREKO. However, the number of DEGs was fourfold increased and the magnitude of response was higher in MREKO vs CO, affecting both gene induction and repression. Taken together our data reveal that, in the cutaneous transcriptional response to GCs mediated through endogenous receptors, epidermal GR is mandatory while epidermal MR acts as a chief modulator of gene expression.

scholarly journals Transcriptional response of BALB/c mouse thyroids following in vivo astatine-211 exposure reveals distinct gene expression profiles

2012 ◽  
Vol 2 (1) ◽  
pp. 32 ◽  
Author(s):  
Nils Rudqvist ◽  
Toshima Z Parris ◽  
Emil Schüler ◽  
Khalil Helou ◽  
Eva Forssell-Aronsson
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptional Response ◽  
Distinct Gene

scholarly journals Gene Expression Profiles for Recurrence of Lymph Node-positive Primary Breast Cancer in Women Over 40 Years of Age

2021 ◽  
Author(s):  
Sean Si Qian Ma ◽  
Luyi Ye ◽  
Fan Zhang ◽  
Tiansheng Xu ◽  
Zai-Si Ji ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Lymph Node ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Olfactory Receptors ◽  
Specific Gene ◽  
Node Metastasis ◽  
Genes Encoding ◽  
Ffpe Samples

Abstract Background: Specific gene expression profiles correlate with recurrence of breast cancer in lymph node-negative patients. In contrast, insufficient knowledge is available regarding tumor-specific gene expression in patients with lymph node metastasis before surgery. Furthermore, such patients experience cumulative incidences of relapse greater than 50%. Methods: Sections of formalin-fixed paraffin embedded (FFPE) were prepared from breast tumors of 37 patients who were followed for at least 5 years. FFPE samples of patients with recurrent ductal breast cancer (n = 25) and 12 FFPE samples of such patients without recurrence were subjected to microarray analysis to identify gene expression profiles specifically associated with positive lymph nodes confirmed during surgery that were accompanied by lymphocytic invasion. Immunohistochemistry was employed to determine the estrogen receptor (ER) status of cancer tissues. All patients were administered tamoxifen after surgery, and this treatment continued for more than 5 years, or until cancer recurred. This strategy eliminated interactions between different therapeutics as potential confounding factors that influenced patients' outcomes.Results: Sixteen genes were expressed at significantly higher levels in patients with ER-positive (+) breast cancer with recurrence compared with those without recurrence. Gene Set Enrichment Analysis of The Kyoto Encyclopedia of Genes and Genomes (KEGG) identified 73 genes encoding olfactory receptors included in the “Olfactory transduction” pathway that were enriched in the ER+ recurrence group (FDR P < 0.05). The KEGG “Histidine metabolism” and “Retinol metabolism” pathways were enriched in patients with ER-negative (–) breast cancer with recurrence (FDR P < 0.05). Conclusions: The present study is the first, to our knowledge, to identify 16 genes encoding proteins with diverse functions as well as 73 genes encoding olfactory receptors. These genes may serve as presurgical biomarkers for the recurrence of ER+ breast cancers with lymph node metastasis before surgery. These findings identify potential therapeutic targets for preventing cancer relapse, particularly after lymph nodes metastasis.

scholarly journals Unraveling Fe(II)-oxidizing mechanisms in a facultative Fe(II) oxidizer Sideroxydans lithotrophicus ES-1 via culturing, transcriptomics, and RT-qPCR

2021 ◽  
Author(s):  
Nanqing Zhou ◽  
Jessica L. Keffer ◽  
Shawn W. Polson ◽  
Clara S Chan
Keyword(s):  
Gene Expression ◽  
Carbon Fixation ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Sulfur Oxidation ◽  
Complex Iii ◽  
Initial Growth ◽  
Gene Expression Response ◽  
Oxidase Gene ◽  
Thiosulfate Oxidation

Sideroxydans lithotrophicus ES-1 grows autotrophically either by Fe(II) oxidation or thiosulfate oxidation, in contrast to most other neutrophilic Fe(II)-oxidizing bacteria (FeOB) isolates. This provides a unique opportunity to explore the physiology of a facultative FeOB and constrain the genes specific to Fe(II) oxidation. We compared the growth of S. lithotrophicus ES-1 on Fe(II), thiosulfate, and both substrates together. While initial growth rates were similar, thiosulfate-grown cultures had higher yield with or without Fe(II) present, which may give ES-1 an advantage over obligate FeOB. To investigate the Fe(II) and S oxidation pathways, we conducted transcriptomics experiments, validated with RT-qPCR. We explored the long-term gene expression response at different growth phases (over days-week) and expression changes during a short-term switch from thiosulfate to Fe(II) (90 min). The dsr and sox sulfur oxidation genes were upregulated in thiosulfate cultures. The Fe(II) oxidase gene cyc2 was among the top expressed genes during both Fe(II) and thiosulfate oxidation, and addition of Fe(II) to thiosulfate-grown cells caused an increase in cyc2 expression. These results support the role of Cyc2 as the Fe(II) oxidase and suggest that ES-1 maintains readiness to oxidize Fe(II) even in the absence of Fe(II). We used gene expression profiles to further constrain the ES-1 Fe(II) oxidation pathway. Notably, among the most highly upregulated genes during Fe(II) oxidation were genes for alternative complex III, reverse electron transport and carbon fixation. This implies a direct connection between Fe(II) oxidation and carbon fixation, suggesting that CO2 is an important electron sink for Fe(II) oxidation.

scholarly journals Testosterone-induced permanent changes of hepatic gene expression in female mice sustained during Plasmodium chabaudi malaria infection

2010 ◽  
Vol 45 (6) ◽  
pp. 379-390 ◽  
Author(s):  
Denis Delić ◽  
Nicole Gailus ◽  
Hans-Werner Vohr ◽  
Mohamed Dkhil ◽  
Saleh Al-Quraishy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Malaria Infection ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Liver Metabolism ◽  
Hepatic Gene Expression ◽  
Plasmodium Chabaudi ◽  
Female Mice ◽  
Genes Encoding

Testosterone has been previously shown to induce persistent susceptibility to Plasmodium chabaudi malaria in otherwise resistant female C57BL/6 mice. Here, we investigate as to whether this conversion coincides with permanent changes of hepatic gene expression profiles. Female mice aged 10–12 weeks were treated with testosterone for 3 weeks; then, testosterone treatment was discontinued for 12 weeks before challenging with 106 P. chabaudi-infected erythrocytes. Hepatic gene expression was examined after 12 weeks of testosterone withdrawal and after subsequent infection with P. chabaudi at peak parasitemia, using Affymetrix microarrays with 22 690 probe sets representing 14 000 genes. The expression of 54 genes was found to be permanently changed by testosterone, which remained changed during malaria infection. Most genes were involved in liver metabolism: the female-prevalent genes Cyp2b9, Cyp2b13, Cyp3a41, Cyp3a44, Fmo3, Sult2a2, Sult3a1, and BC014805 were repressed, while the male-prevalent genes Cyp2d9, Cyp7b1, Cyp4a10, Ugt2b1, Ugt2b38, Hsd3b5, and Slco1a1 were upregulated. Genes encoding different nuclear receptors were not persistently changed. Moreover, testosterone induced persistent upregulation of genes involved in hepatocellular carcinoma such as Lama3 and Nox4, whereas genes involved in immune response such as Ifnγ and Igk-C were significantly decreased. Our data provide evidence that testosterone is able to induce specific and robust long-term changes of gene expression profiles in the female mouse liver. In particular, those changes, which presumably indicate masculinized liver metabolism and impaired immune response, may be critical for the testosterone-induced persistent susceptibility of mice to P. chabaudi malaria.

scholarly journals Global Gene Expression Responses to Cadmium Toxicity in Escherichia coli

2005 ◽  
Vol 187 (9) ◽  
pp. 3259-3266 ◽  
Author(s):  
Anyou Wang ◽  
David E. Crowley
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Ribosomal Proteins ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Cadmium Toxicity ◽  
Gene Expression Profiles ◽  
Global Gene Expression ◽  
Temporal Gene Expression ◽  
Genes Encoding

ABSTRACT Genome-wide analysis of temporal gene expression profiles in Escherichia coli following exposure to cadmium revealed a shift to anaerobic metabolism and induction of several stress response systems. Disruption in the transcription of genes encoding ribosomal proteins and zinc-binding proteins may partially explain the molecular mechanisms of cadmium toxicity.

scholarly journals Psychological resilience and the gene regulatory impact of posttraumatic stress in Nepali child soldiers

2016 ◽  
Vol 113 (29) ◽  
pp. 8156-8161 ◽  
Author(s):  
Brandon A. Kohrt ◽  
Carol M. Worthman ◽  
Ramesh P. Adhikari ◽  
Nagendra P. Luitel ◽  
Jesusa M. G. Arevalo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Posttraumatic Stress ◽  
Early Life ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptional Response ◽  
Child Soldiers ◽  
Psychological Resilience ◽  
Early Life Adversity ◽  
Former Child Soldiers

Adverse social conditions in early life have been linked to increased expression of proinflammatory genes and reduced expression of antiviral genes in circulating immune cells—the conserved transcriptional response to adversity (CTRA). However, it remains unclear whether such effects are specific to the Western, educated, industrialized, rich, and democratic (WEIRD) cultural environments in which previous research has been conducted. To assess the roles of early adversity and individual psychological resilience in immune system gene regulation within a non-WEIRD population, we evaluated CTRA gene-expression profiles in 254 former child soldiers and matched noncombatant civilians 5 y after the People’s War in Nepal. CTRA gene expression was up-regulated in former child soldiers. These effects were linked to the degree of experienced trauma and associated distress—that is, posttraumatic stress disorder (PTSD) severity—more than to child soldier status per se. Self-perceived psychological resilience was associated with marked buffering of CTRA activation such that PTSD-affected former child soldiers with high levels of personal resilience showed molecular profiles comparable to those of PTSD-free civilians. These results suggest that CTRA responses to early life adversity are not restricted to WEIRD cultural contexts and they underscore the key role of resilience in determining the molecular impact of adverse environments.

Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart

2012 ◽  
Vol 302 (9) ◽  
pp. H1826-H1837 ◽  
Author(s):  
Monica Forero McGrath ◽  
Tsuneo Ogawa ◽  
Adolfo J. de Bold
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Hormone Secretion ◽  
Gene Expression Profiles ◽  
Transcriptional Response ◽  
Volume Overload ◽  
Inhibitory Protein ◽  
Therapeutic Implications ◽  
Molecular Events

Because of the crucial role of the endocrine heart in maintaining homeostasis, considerable effort has been focused on the elucidation of the mechanistic underlying gene expression and secretion of the cardiac hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP). However, much remains to be determined regarding specific molecular events involved in cardiocyte secretory function. In this work, we identified genes involved in the transcriptional response of the endocrine heart to volume overload (VO) and signaling pathways involved in its regulation. To this end, the cardiac atrial and ventricular transcriptomes were analyzed in the heart of rats subjected to experimentally induced aorto-caval shunt VO. Pathway analysis revealed unique gene expression profiles in the VO atria for G-protein signaling, notably a significant downregulation of Ras dexamethasone-induced protein 1 (RASD1). In vitro, knockdown of RASD1 in the atrial-derived HL-1 cells, significantly increased ANF secretion. Concurrent knockdown of RASD1 and its effectors Gαo1 or Gβ1γ2 abrogated the endocrine response, demonstrating a previously unknown negative modulator role for RASD1. RASD1 thus emerges as a tonic inhibitor of ANF secretion and illustrates for the first time the concept of inhibitory protein regulators of ANF release. The novel molecular function identified herein for RASD1 is of considerable importance given its therapeutic implications for cardiovascular disease.

scholarly journals Brucella melitensis Triggers Time-Dependent Modulation of Apoptosis and Down-Regulation of Mitochondrion-Associated Gene Expression in Mouse Macrophages

2006 ◽  
Vol 74 (9) ◽  
pp. 5035-5046 ◽  
Author(s):  
Yongqun He ◽  
Sherry Reichow ◽  
Sheela Ramamoorthy ◽  
Xicheng Ding ◽  
Raju Lathigra ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brucella Melitensis ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptional Response ◽  
Necrosis Factor Alpha ◽  
Mitochondrial Functions ◽  
Mouse Macrophages ◽  
External Stimuli ◽  
Infection Stage

ABSTRACT Brucella spp. are facultative intracellular bacteria that cause brucellosis in humans and other animals. Brucella spp. are taken up by macrophages, and the outcome of the macrophage-Brucella interaction is a basis for establishment of a chronic Brucella infection. Microarrays were used to analyze the transcriptional response of the murine macrophage-like J774.A1 cell line to infection with virulent Brucella melitensis strain 16M. It was found that most significant changes in macrophage gene transcription happened early following infection, and global macrophage gene expression profiles returned to normal between 24 and 48 h postinfection. These findings support the observation that macrophages kill the majority of Brucella cells at the early infection stage, but the surviving Brucella cells are able to avoid macrophage brucellacidal activity inside replicative phagosomes at the later infection stage. At 4 h postinfection, macrophage genes involved in cell growth, metabolism, and responses to endogenous stimuli were down-regulated, while the inflammatory response (e.g., tumor necrosis factor alpha and Toll-like receptor 2), the complement system, the responses to external stimuli, and other immune responses were up-regulated. It is likely that the most active brucellacidal activity happened between 0 and 4 h postinfection. Mitochondrion-associated gene expression, which is involved in protein synthesis and transport, electron transfer, and small-molecule transfer, and many other mitochondrial functions were significantly down-regulated at 4 h postinfection. Although there were both pro- and antiapoptosis effects, B. melitensis 16M appears to inhibit apoptosis of macrophages by blocking release of cytochrome c and production of reactive oxygen species in the mitochondria, thus preventing activation of caspase cascades.

scholarly journals Histone H3.3 G34 mutations promote aberrant PRC2 activity and drive tumor progression

2020 ◽  
Vol 117 (44) ◽  
pp. 27354-27364 ◽  
Author(s):  
Siddhant U. Jain ◽  
Sima Khazaei ◽  
Dylan M. Marchione ◽  
Stefan M. Lundgren ◽  
Xiaoshi Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Tumor Development ◽  
Gene Expression Profiles ◽  
Osteoblastic Differentiation ◽  
Missense Mutations ◽  
Giant Cell Tumors ◽  
H3k36 Methylation ◽  
Genes Encoding

A high percentage of pediatric gliomas and bone tumors reportedly harbor missense mutations at glycine 34 in genes encoding histone variant H3.3. We find that these H3.3 G34 mutations directly alter the enhancer chromatin landscape of mesenchymal stem cells by impeding methylation at lysine 36 on histone H3 (H3K36) by SETD2, but not by the NSD1/2 enzymes. The reduction of H3K36 methylation by G34 mutations promotes an aberrant gain of PRC2-mediated H3K27me2/3 and loss of H3K27ac at active enhancers containing SETD2 activity. This altered histone modification profile promotes a unique gene expression profile that supports enhanced tumor development in vivo. Our findings are mirrored in G34W-containing giant cell tumors of bone where patient-derived stromal cells exhibit gene expression profiles associated with early osteoblastic differentiation. Overall, we demonstrate that H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism by which H3.3 G34 mutations drive these tumors.

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