scholarly journals Environmental and evolutionary drivers of the modular gene regulatory network underlying phenotypic plasticity for stress resistance in the nematode Caenorhabditis remanei

2018 ◽  
Author(s):  
Kristin L. Sikkink ◽  
Rose M. Reynolds ◽  
Catherine M. Ituarte ◽  
William A. Cresko ◽  
Patrick C. Phillips
Keyword(s):  
Heat Stress ◽  
Phenotypic Plasticity ◽  
Transcriptional Response ◽  
Molecular Networks ◽  
Ancestral Population ◽  
Plastic Response ◽  
Transcriptional Responses ◽  
Acute Heat Stress ◽  
Environmental Responses ◽  
Caenorhabditis Remanei

ABSTRACTIn response to changing environmental conditions, organisms can acclimate through phenotypic plasticity or adapt by evolving mechanisms to cope with novel stressors. Changes in gene expression, whether dynamic or evolved, are an important way in which environmental responses are mediated; however, much is still unknown about how the molecular networks underlying plastic phenotypes evolve. Here, we compare transcriptional responses to acute heat stress among four populations of the nematode Caenorhabditis remanei—one selected to withstand heat stress, one selected under oxidative stress, an unselected control, and the ancestral population. We used a weighted gene coexpression network analysis within these lines to identify transcriptional modules, which are sets of genes that respond similarly to stress via plastic responses, evolutionary responses, or both. The transcriptional response to acute heat stress is dominated by a plastic response that is shared in the ancestor and all evolved populations. However, we also identified several modules that respond to artificial selection by (1) changing the baseline level of expression, (2) altering the magnitude of the plastic response, or (3) a combination of the two. Our findings reveal that while it is possible to perturb the nature of the transcriptional response network with short bouts of intense selection, the overall structure of transcriptional plasticity is dominated by inherent, ancestral regulatory systems.

The transcriptional response of the Pacific oyster Crassostrea gigas against acute heat stress

2017 ◽  
Vol 68 ◽  
pp. 132-143 ◽  
Author(s):  
Chuanyan Yang ◽  
Qiang Gao ◽  
Chang Liu ◽  
Lingling Wang ◽  
Zhi Zhou ◽  
...  
Keyword(s):  
Heat Stress ◽  
Crassostrea Gigas ◽  
Pacific Oyster ◽  
Transcriptional Response ◽  
Acute Heat Stress ◽  
The Pacific

scholarly journals The protein modifier SUMO is critical for Arabidopsis shoot meristem maintenance at warmer ambient temperatures

2021 ◽  
Author(s):  
Valentin Hammoudi ◽  
Bas Beerens ◽  
Martijs J. Jonker ◽  
Tieme A. Helderman ◽  
Georgios Vlachakis ◽  
...  
Keyword(s):  
Heat Stress ◽  
Protein Modification ◽  
Heat Waves ◽  
Transcriptional Response ◽  
Shoot Meristem ◽  
Ambient Temperatures ◽  
Sumo Proteases ◽  
Acute Heat Stress ◽  
Meristem Development ◽  
Meristem Maintenance

AbstractShort heat waves (>37°C) are extremely damaging to non-acclimated plants and their capacity to recover from heat stress is key for their survival. To acclimate, the HEAT SHOCK TRANSCRIPTION FACTOR A1 (HSFA1) subfamily activates a transcriptional response that resolves incurred damages. In contrast, little is known how plants acclimate to sustained non-detrimental warm periods at 27-28°C. Plants respond to this condition with a thermomorphogenesis response. In addition, HSFA1 is critical for plant survival during these warm periods. We find that SUMO, a protein modification whose conjugate levels rise sharply during acute heat stress in eukaryotes, is critical too for plant longevity during warm periods, in particular for normal shoot meristem development. The known SUMO ligases were not essential to endure these warm periods, alone or in combination. Thermo-lethality was also not seen when plants lacked certain SUMO proteases or when SUMO chain formation was blocked. The SUMO-dependent thermo-resilience was as well independent of the autoimmune phenotype of the SUMO mutants. As acquired thermotolerance was normal in the sumo1/2 knockdown mutant, our data thus reveal a role for SUMO in heat acclimation that differs from HSFA1 and SIZ1. We conclude that SUMO is critical for shoot meristem integrity during warm periods.HighlightThe protein modifier SUMO governs shoot meristem maintenance in Arabidopsis allowing sustained rosette development when plants endure a sustained warm non-detrimental period of 28 degrees Celsius.

High Altitude hypoxia

2020 ◽  
Vol 17 ◽  
Author(s):  
Asma Babar ◽  
Kifayatullah Mengal ◽  
Abdul Hanan Babar ◽  
Shixin Wu ◽  
Mujahid Ali Shah ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
High Altitude ◽  
Molecular Mechanisms ◽  
Strong Association ◽  
Haemoglobin Concentration ◽  
Metabolic Reprogramming ◽  
Molecular Networks ◽  
Whole Genome ◽  
Gene Expressions ◽  
Transcriptional Responses

: The world highest and largest altitude area is called the Qinghai-Tibetan plateau (QTB), which harbors unique animal and plant species. Mammals that inhabit the higher altitude regions have adapted well to the hypoxic conditions. One of the main stressors at high altitude is hypoxia. Metabolic responses to hypoxia play important roles in cell survival strategies and some diseases. However, the homeostatic alterations that equilibrate variations in the demand and supply of energy to maintain organismal function in a prolonged low O2 environment persist partly understood, making it problematic to differentiate adaptive from maladaptive responses in hypoxia. Tibetans and yaks are two perfect examples innate to the plateau for high altitude adaptation. By the scan of the whole-genome, EPAS1 and EGLN1 were identified as key genes associated with sustained haemoglobin concentration in high altitude mammals for adaptation. The yak is a much more ancient mammal which has existed on QTB longer than humans, it is, therefore, possible that natural selection represented a diverse group of genes/pathways in yaks. Physiological characteristics are extremely informative in revealing molecular networks associated with inherited adaptation, in addition to the whole-genome adaptive changes at the DNA sequence level. Gene-expression can be changed by a variety of signals originating from the environment, and hypoxia is the main factor amongst them. The hypoxia-inducible factors (HIF-1α and EPAS1/HIF-2α) are the main regulators of oxygen in homeostasis which play a role as maestro regulators of adaptation in hypoxic reaction of molecular mechanisms. (Vague) The basis of this review is to present recent information regarding the molecular mechanism involved in hypoxia that regulates candidate genes and proteins. Many transcriptional responses toward hypoxia are facilitated by HIFs that change the number of gene expressions and help in angiogenesis, erythropoiesis, metabolic reprogramming and metastasis. HIFs also activate several signals highlighting a strong association between hypoxia, the misfolded proteins’ accumulation in the endoplasmic reticulum in stress and activation of unfolded protein response (UPR). It was observed that at high-altitude, pregnancies yield a low birth weight ∼100 g per1000 m of the climb. (Vague) It may involve variation in the events of energy-demanding, like protein synthesis. Prolonged hypobaric hypoxia causes placental ER stress, which in turn, moderates protein synthesis and reduces proliferation. Further, Cardiac hypertrophy by cytosolic Ca2+ raises and Ca2+/calmodulin, calcineurin stimulation, NF-AT3 pathway might be caused by an imbalance in Sarcoplasmic reticulum ER Ca2, might be adaptive in beginning but severe later.

Repeated thermal conditioning during the neonatal period affects behavioral and physiological responses to acute heat stress in chicks

2020 ◽  
Vol 94 ◽  
pp. 102759
Author(s):  
Yoshimitsu Ouchi ◽  
Hiroshi Tanizawa ◽  
Jun-ichi Shiraishi ◽  
John F. Cockrem ◽  
Vishwajit S. Chowdhury ◽  
...  
Keyword(s):  
Heat Stress ◽  
Neonatal Period ◽  
Physiological Responses ◽  
Acute Heat Stress

scholarly journals Evaluation of physiological and molecular responses to acute heat stress in two chicken breeds

animal ◽  
2020 ◽  
pp. 100106
Author(s):  
P. Adu-Asiamah ◽  
Y. Zhang ◽  
K. Amoah ◽  
Q.Y. Leng ◽  
J.H. Zheng ◽  
...  
Keyword(s):  
Heat Stress ◽  
Molecular Responses ◽  
Acute Heat Stress ◽  
Chicken Breeds

scholarly journals Dynamic Responses to Acute Heat Stress between 34 °C and 38.5 °C, and Characteristics of Heat Stress Response in Mice

2003 ◽  
Vol 26 (5) ◽  
pp. 701-708 ◽  
Author(s):  
Naoki Harikai ◽  
Kanji Tomogane ◽  
Mitsue Miyamoto ◽  
Keiko Shimada ◽  
Satoshi Onodera ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Dynamic Responses ◽  
Heat Stress Response ◽  
Acute Heat Stress

scholarly journals Tumor hypoxia induces nuclear paraspeckle formation through HIF-2α dependent transcriptional activation of NEAT1 leading to cancer cell survival

Oncogene ◽  
2014 ◽  
Vol 34 (34) ◽  
pp. 4482-4490 ◽  
Author(s):  
H Choudhry ◽  
A Albukhari ◽  
M Morotti ◽  
S Haider ◽  
D Moralli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Transcriptional Activation ◽  
Cellular Proliferation ◽  
Hypoxia Inducible Factor ◽  
Tumor Hypoxia ◽  
Transcriptional Response ◽  
Clonogenic Survival ◽  
Breast Cancer Cell Lines ◽  
Transcriptional Responses

Abstract Activation of cellular transcriptional responses, mediated by hypoxia-inducible factor (HIF), is common in many types of cancer, and generally confers a poor prognosis. Known to induce many hundreds of protein-coding genes, HIF has also recently been shown to be a key regulator of the non-coding transcriptional response. Here, we show that NEAT1 long non-coding RNA (lncRNA) is a direct transcriptional target of HIF in many breast cancer cell lines and in solid tumors. Unlike previously described lncRNAs, NEAT1 is regulated principally by HIF-2 rather than by HIF-1. NEAT1 is a nuclear lncRNA that is an essential structural component of paraspeckles and the hypoxic induction of NEAT1 induces paraspeckle formation in a manner that is dependent upon both NEAT1 and on HIF-2. Paraspeckles are multifunction nuclear structures that sequester transcriptionally active proteins as well as RNA transcripts that have been subjected to adenosine-to-inosine (A-to-I) editing. We show that the nuclear retention of one such transcript, F11R (also known as junctional adhesion molecule 1, JAM1), in hypoxia is dependent upon the hypoxic increase in NEAT1, thereby conferring a novel mechanism of HIF-dependent gene regulation. Induction of NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and reduced apoptosis, all of which are hallmarks of increased tumorigenesis. Furthermore, in patients with breast cancer, high tumor NEAT1 expression correlates with poor survival. Taken together, these results indicate a new role for HIF transcriptional pathways in the regulation of nuclear structure and that this contributes to the pro-tumorigenic hypoxia-phenotype in breast cancer.

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