scholarly journals Pseudocrossidium replicatum (Taylor) R.H. Zander is a fully desiccation-tolerant moss that expresses an inducible molecular mechanism in response to severe abiotic stress

Author(s):  
Selma Ríos-Meléndez ◽  
Emmanuel Valadez-Hernández ◽  
Claudio Delgadillo ◽  
Maria L. Luna-Guevara ◽  
Mario A. Martínez-Núñez ◽  
...  

Abstract Key message The moss Pseudocrossidium replicatum is a desiccation-tolerant species that uses an inducible system to withstand severe abiotic stress in both protonemal and gametophore tissues. Abstract Desiccation tolerance (DT) is the ability of cells to recover from an air-dried state. Here, the moss Pseudocrossidium replicatum was identified as a fully desiccation-tolerant (FDT) species. Its gametophores rapidly lost more than 90% of their water content when exposed to a low-humidity atmosphere [23% relative humidity (RH)], but abscisic acid (ABA) pretreatment diminished the final water loss after equilibrium was reached. P. replicatum gametophores maintained good maximum photosystem II (PSII) efficiency (Fv/Fm) for up to two hours during slow dehydration; however, ABA pretreatment induced a faster decrease in the Fv/Fm. ABA also induced a faster recovery of the Fv/Fm after rehydration. Protein synthesis inhibitor treatment before dehydration hampered the recovery of the Fv/Fm when the gametophores were rehydrated after desiccation, suggesting the presence of an inducible protective mechanism that is activated in response to abiotic stress. This observation was also supported by accumulation of soluble sugars in gametophores exposed to ABA or NaCl. Exogenous ABA treatment delayed the germination of P. replicatum spores and induced morphological changes in protonemal cells that resembled brachycytes. Transcriptome analyses revealed the presence of an inducible molecular mechanism in P. replicatum protonemata that was activated in response to dehydration. This study is the first RNA-Seq study of the protonemal tissues of an FDT moss. Our results suggest that P. replicatum is an FDT moss equipped with an inducible molecular response that prepares this species for severe abiotic stress and that ABA plays an important role in this response.

2014 ◽  
Vol 307 (11) ◽  
pp. E1047-E1056 ◽  
Author(s):  
Xiaodong Zhang ◽  
Bradlee L. Heckmann ◽  
Xitao Xie ◽  
Alicia M. Saarinen ◽  
Jun Liu

Fat-specific protein 27 (FSP27) plays a pivotal role in controlling the formation of large lipid droplet and energy metabolism. The cellular levels of FSP27 are tightly regulated through the proteasomal ubiquitin-mediated degradation. However, the upstream signals that trigger FSP27 degradation and the underlying mechanism(s) have yet to be identified. Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-β-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. The levels of FSP27 protein could be maintained by either knocking down AMPKα1 or blocking proteasomal pathway. Moreover, AICAR treatment induced multilocularization of LDs in 3T3-L1 adipocytes, reminiscent of the morphological changes in cells depleted of FSP27. Furthermore, mass spectrometry-based proteomic analysis identified heat shock cognate 70 (HSC70) as a novel binding protein of FSP27. The specific interaction was confirmed by co-immunoprecipitation of both ectopically expressed and endogenous proteins. Importantly, knockdown of HSC70 by small interference RNA resulted in increased half-life of FSP27 in cells treated with a protein synthesis inhibitor cycloheximide (CHX) or AICAR. However, silencing of the E3 ubiquitin ligase CHIP (COOH terminus of HSC70-interacting protein) failed to alter the stability of FSP27 protein under both conditions. Taken together, our data indicate that AMPK is a negative regulator of FSP27 stability through the proteasomal ubiquitin-dependent protein catabolic process. Promotion of FSP27 degradation may be an important factor responsible for the beneficial effect of AMPK activators on energy metabolism.


Agronomy ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1579
Author(s):  
Qari Muhammad Imran ◽  
Noreen Falak ◽  
Adil Hussain ◽  
Bong-Gyu Mun ◽  
Byung-Wook Yun

Plants, due to their sessile nature, face several environmental adversities. Abiotic stresses such as heat, cold, drought, heavy metals, and salinity are serious threats to plant production and yield. To cope with these stresses, plants have developed sophisticated mechanisms to avoid or resist stress conditions. A proper response to abiotic stress depends primarily on how plants perceive the stress signal, which in turn leads to initiation of signaling cascades and induction of resistance genes. New biotechnological tools such as RNA-seq and CRISPR-cas9 are quite useful in identifying target genes on a global scale, manipulating these genes to achieve tolerance, and helping breeders to develop stress-tolerant cultivars. In this review, we will briefly discuss the adverse effects of key abiotic stresses such as cold, heat, drought, and salinity. We will also discuss how plants sense various stresses and the importance of biotechnological tools in the development of stress-tolerant cultivars.


1986 ◽  
Vol 55 (03) ◽  
pp. 369-374 ◽  
Author(s):  
Raffaele De Caterina ◽  
Babette B Weksler

SummaryTo learn whether glucocorticoids inhibit prostaglandin (PG) production in vascular endothelial cells, we investigated the effects of glucocorticoids on PG synthesis by cultured human umbilical vein endothelial cells (EC). Pretreatment of EC with dexamethasone (DX, 10-9 to 5 x 10-5 M) caused a dose-dependent inhibition of PGI2 production when PG synthesis from endogenous arachidonate was stimulated by human thrombin (0.25-2 U/ml) or ionophore A 23187 (1-5 μM). The inhibition was detectable at 10-7 M DX and maximal at 10-5 M (4.0 ± 0.7 vs. control: 7.7 ± 1.9 ng/ml, mean ± S.D., P <0.01). The production of PGE2 and the release of radiolabelled arachidonate (AA) from prelabelled cells were similarly inhibited. Prolonged incubation of EC with glucocorticoids was required to inhibit PG production or arachidonate release: ranging from 8% inhibition at 5 h to 44% at 38 h. In contrast, prostaglandin formation from exogenous AA was not altered by DX treatment. When thrombin or ionophore-stimulated EC were restimulated with exogenous AA (25 μM), DX-treated cells released more PGI2 than control cells (5.7 ± 0.5 vs. 4.1 ± 0.6 ng/ml, P <0.01). Both the decrease in PGI2 production after thrombin/ionophore and the increase after re-stimulation with AA were blunted in the presence of the protein synthesis inhibitor cycloheximide (0.1-0.2 μg/ml). Thus, incubation of EC with glucocorticoids inhibits PG production at the step of phospholipase activation. The time requirement for these steroid effects and their blunting by cycloheximide are consistent with the induction of regulatory proteins, possibly lipocortins, in endothelial cells.


1983 ◽  
Vol 45 (1) ◽  
pp. 452-455 ◽  
Author(s):  
F Ben-Hamida ◽  
A Person ◽  
G Beaud

Author(s):  
Daiane Carvalho Baía ◽  
Fábio L. Olivares ◽  
Daniel B. Zandonadi ◽  
Cleiton de Paula Soares ◽  
Riccardo Spaccini ◽  
...  

Abstract Background Plants primed by humic acids showed physiological and molecular response against different abiotic stresses without the presence of stressor agents (salinity, drought, heavy metal toxicity). It is plausible that humic acids themselves can act as chemical priming substances in plants. We hypothesized that humic acids can trigger the weak acids stress response in cell plants acidifying the cytosol and thus eliciting the transduction signalling response cascade. Methods The dose–response curves of maize seedlings roots with different concentrations of humic, acetic and salicylic acids determined the most active and inhibitory concentration. These data were further used to evaluate changes on intracellular pH using BCECF-AM probe (2,7-bis(2-carboxyethyl)-5(and 6)-carboxyfluorescein, acetoxymethyl ester) and differential transcription level of genes related to weak stress response in plants by qPCR real time. Results Humic acids like short chain organic acids decrease the intracellular pH showed by the increased fluorescence of BCECF probe. The drop in cytosolic pH promoted by humic acids was not transient. We observed a high level of protein kinases related to cell energy-sensing and transcription factors associated to transduction of stress signalling. Conclusion The humic acids can be considered as a chemical priming agent, since in the appropriate concentration they can induce the typical plant abiotic stress response of weak acids inducing plant acclimation and enhancing the abiotic stress tolerance.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Huahe Zhu ◽  
Shun Wang ◽  
Cong Shan ◽  
Xiaoqian Li ◽  
Bo Tan ◽  
...  

AbstractXuan-bai-cheng-qi decoction (XCD), a traditional Chinese medicine (TCM) prescription, has been widely used to treat a variety of respiratory diseases in China, especially to seriously infectious diseases such as acute lung injury (ALI). Due to the complexity of the chemical constituent, however, the underlying pharmacological mechanism of action of XCD is still unclear. To explore its protective mechanism on ALI, firstly, a network pharmacology experiment was conducted to construct a component-target network of XCD, which identified 46 active components and 280 predicted target genes. Then, RNA sequencing (RNA-seq) was used to screen differentially expressed genes (DEGs) between ALI model rats treated with and without XCD and 753 DEGs were found. By overlapping the target genes identified using network pharmacology and DEGs using RNA-seq, and subsequent protein–protein interaction (PPI) network analysis, 6 kernel targets such as vascular epidermal growth factor (VEGF), mammalian target of rapamycin (mTOR), AKT1, hypoxia-inducible factor-1α (HIF-1α), and phosphoinositide 3-kinase (PI3K) and gene of phosphate and tension homology deleted on chromsome ten (PTEN) were screened out to be closely relevant to ALI treatment. Verification experiments in the LPS-induced ALI model rats showed that XCD could alleviate lung tissue pathological injury through attenuating proinflammatory cytokines release such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β. Meanwhile, both the mRNA and protein expression levels of PI3K, mTOR, HIF-1α, and VEGF in the lung tissues were down-regulated with XCD treatment. Therefore, the regulations of XCD on PI3K/mTOR/HIF-1α/VEGF signaling pathway was probably a crucial mechanism involved in the protective mechanism of XCD on ALI treatment.


2006 ◽  
Vol 23 (2) ◽  
pp. 43-46
Author(s):  
Kiyotaka Matsumura ◽  
Manami Nagano ◽  
Sachiko Tsukamoto ◽  
Haruko Kato ◽  
Nobuhiro Fusetani

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