scholarly journals Meta-analysis of the General Coral Stress Response: Acropora corals show opposing responses depending on stress intensity

2019 ◽  
Author(s):  
Groves Dixon ◽  
Evelyn Abbott ◽  
Mikhail Matz

AbstractAs climate change progresses, reef-building corals must contend more often with suboptimal conditions, motivating a need to understand coral stress response. Here we test the hypothesis that there is a stereotyped transcriptional response that corals enact under any stressful conditions, functionally characterized by downregulation of growth and activation of cell death, response to reactive oxygen species, immunity, and protein homeostasis. We analyze RNA-seq and Tag-Seq data from 14 previously published studies and supplement them with four new experiments involving different stressors, totaling over 600 gene expression profiles from the genus Acropora. Contrary to expectations, we found not one, but two distinct types of response. The type A response was observed under all kinds of high-intensity stress, showed strong correlations between independent projects, and was functionally consistent with the hypothesized stereotyped response. Higher similarity of type A responses irrespective of stress type supports its role as the General Coral Stress Response providing a blanket solution to severely stressful conditions. The distinct type B response was observed under lower intensity stress and was weaker and more variable among studies than type A. Unexpectedly, the type B response was broadly opposite the type A response: biological processes up-regulated under type A response tended to be down-regulated under type B response, and vice versa. Gene network analysis indicated that type B response does not involve specific co-regulated gene groups and is simply the opposite of type A response. We speculate that these paradoxically opposing responses may result from an inherent negative association between stress response and cell proliferation.


2021 ◽  
Author(s):  
Laura Puente-Santamaria ◽  
Lucia Sanchez-Gonzalez ◽  
Ricardo Ramos-Ruiz ◽  
Luis del Peso

Molecular gene signatures are useful tools to characterize the physiological state of cell populations according to their gene expression profiles. However, most molecular gene signatures have been developed under a very limited set of conditions and cell types, and are often restricted to a set of gene identities linked to an event or biological process, therefore making necessary to develop and test additional procedures for its application to new data. Focusing on the transcriptional response to hypoxia, we aimed to generate widely applicable classifiers capable of detecting hypoxic samples while maintaining transparency and ease of use and interpretation. Here we describe several tree-based classifiers sourced from the results of a meta-analysis of 69 differential expression datasets which included 425 individual RNA-seq experiments from 33 different human cell types exposed to different degrees of hypoxia (0.1-5%O2) for a time spanning between 2 and 48h. These decision trees include both the identities of genes key in the response to hypoxia and defined quantitative boundaries, allowing for the classification of individual samples without needing a control or normoxic reference. Despite their simplicity and ease of use, these classifiers achieve over 95% accuracy in cross validation and over 80% accuracy when applied to additional challenging datasets. Moreover, the explicit structure of the trees allowed for the identification of relevant biological features in cases where prediction was not accurate. Finally, we demonstrate that the classifiers can be applied to spatial gene expression data to identify hypoxic regions within histological sections. Although we have focused on the identification of hypoxia, this method can be applied to detect activation of other processes or cellular states.



2009 ◽  
Vol 8 (4) ◽  
pp. 207-214 ◽  
Author(s):  
An-Ting T. Lu ◽  
Shelley R. Salpeter ◽  
Anthony E. Reeve ◽  
Steven Eschrich ◽  
Patrick G. Johnston ◽  
...  


BMC Genomics ◽  
2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Robin Kosch ◽  
Julien Delarocque ◽  
Peter Claus ◽  
Stefanie C. Becker ◽  
Klaus Jung


2022 ◽  
Vol 56 ◽  
pp. 39-49
Author(s):  
Ignazio S Piras ◽  
Matthew J. Huentelman ◽  
Federica Pinna ◽  
Pasquale Paribello ◽  
Marco Solmi ◽  
...  


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Lisa M. Sevilla ◽  
Judit Bigas ◽  
Álvaro Chiner-Oms ◽  
Iñaki Comas ◽  
Vicente Sentandreu ◽  
...  

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.



Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1992
Author(s):  
Andrea Moerman-Herzog ◽  
Syed J. Mehdi ◽  
Henry K. Wong

Sézary syndrome (SS), an aggressive cutaneous T-cell lymphoma (CTCL) with poor prognosis, is characterized by the clinical hallmarks of circulating malignant T cells, erythroderma and lymphadenopathy. However, highly variable clinical skin manifestations and similarities with benign mimickers can lead to significant diagnostic delay and inappropriate therapy that can lead to disease progression and mortality. SS has been the focus of numerous transcriptomic-profiling studies to identify sensitive and specific diagnostic and prognostic biomarkers. Benign inflammatory disease controls (e.g., psoriasis, atopic dermatitis) have served to identify chronic inflammatory phenotypes in gene expression profiles, but provide limited insight into the lymphoproliferative and oncogenic roles of abnormal gene expression in SS. This perspective was recently clarified by a transcriptome meta-analysis comparing SS and lymphocytic-variant hypereosinophilic syndrome, a benign yet often clonal T-cell lymphoproliferation, with clinical features similar to SS. Here we review the rationale for selecting lymphocytic-variant hypereosinophilic syndrome (L-HES) as a disease control for SS, and discuss differentially expressed genes that may distinguish benign from malignant lymphoproliferative phenotypes, including additional context from prior gene expression studies to improve understanding of genes important in SS.



2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Sun Young Lee ◽  
Yong Kwang Park ◽  
Cheol-Hee Yoon ◽  
Kisoon Kim ◽  
Kyung-Chang Kim


Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 12755-12766 ◽  
Author(s):  
Somsak Likhitrattanapisal ◽  
Jaitip Tipanee ◽  
Tavan Janvilisri


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