The involvement of gaseous signaling molecules in plant MAPK cascades: function and signal transduction

Planta ◽  
2021 ◽  
Vol 254 (6) ◽  
Author(s):  
Xuetong Wu ◽  
Zhiya Liu ◽  
Weibiao Liao
Physiology ◽  
1997 ◽  
Vol 12 (6) ◽  
pp. 286-293 ◽  
Author(s):  
JT Neary

Distinct signal transduction cascades comprised of at least three proteinkinases mediate cellular proliferation and differentiation, growth arrest, and programmed cell death. These cytosolic enzymes relay extracellular signals from cell surface to nucleus, leading to changes in gene expression. Signaling components of these cascades offer new possibilities for therapeutic strategies in tumorigenesis, inflammatory diseases, immunopotentiation, wound healing, and regeneration.


Plants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2611
Author(s):  
Jong Hee Im ◽  
Seungmin Son ◽  
Jae-Heung Ko ◽  
Kyung-Hwan Kim ◽  
Chung Sun An ◽  
...  

The plant mitogen-activated protein kinase (MPK) cascade, a highly conserved signal transduction system in eukaryotes, plays a crucial role in the plant’s response to environmental stimuli and phytohormones. It is well-known that nuclear translocation of MPKs is necessary for their activities in mammalian cells. However, the mechanism underlying nuclear translocation of plant MPKs is not well elucidated. In the previous study, it has been shown that soybean MPK6 (GmMPK6) is activated by phosphatidic acid (PA) and hydrogen peroxide (H2O2), which are two signaling molecules generated during salt stress. Using the two signaling molecules, we investigated how salt stress triggers its translocation to the nucleus. Our results show that the translocation of GmMPK6 to the nucleus is mediated by H2O2, but not by PA. Furthermore, the translocation was interrupted by diphenylene iodonium (DPI) (an inhibitor of RBOH), confirming that H2O2 is the signaling molecule for the nuclear translocation of GmMPK6 during salt stress.


2020 ◽  
Vol 11 (20) ◽  
pp. 5127-5141 ◽  
Author(s):  
Mingwang Yang ◽  
Jiangli Fan ◽  
Jianjun Du ◽  
Xiaojun Peng

This perspective article aims to introduce the design principles and recognition strategies of small-molecule fluorescent probes which are applied for the detection of gas signaling molecules including NO, CO and H2S in biological systems.


Science ◽  
2016 ◽  
Vol 352 (6285) ◽  
pp. 595-599 ◽  
Author(s):  
Xiaolei Su ◽  
Jonathon A. Ditlev ◽  
Enfu Hui ◽  
Wenmin Xing ◽  
Sudeep Banjade ◽  
...  

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 800-800
Author(s):  
Roberto Negro ◽  
Pablo G Longo ◽  
Michela Tarnani ◽  
Stefania Gobessi ◽  
Luca Laurenti ◽  
...  

Abstract Abstract 800 CLL B cells display many features that suggest a role for antigen stimulation in the development and progression of the disease. These include the expression of stereotyped B-cell receptors (BCRs), the association between IgVH gene mutation status and prognosis, and the gene-expression profile of antigen-stimulated B cells. In addition, CLL B cells have other BCR-related features that distinguish them from normal B lymphocytes, such as lower levels of surface Ig, less efficient BCR signal transduction and increased basal activity of the proximal BCR signaling molecules Lyn and Syk. We have now investigated whether any of these features are related to aberrant expression or function of the phosphatases SHP-1, SHP-2 and Lyp (PTPN22), which regulate the amplitude and duration of the BCR signal by dephosphorylating various components of the BCR signal transduction unit. These phosphatases are also interesting because mutated or polymorphic variants have been linked to various malignant or autoimmune diseases. We started our study by performing nucleotide sequence analysis of the complete coding region of SHP1, SHP2 and Lyp in 8, 21 and 29 CLL B cell samples, respectively. Overall, only two mutations were identified (an R527C substitution in SHP2 and a Q456E substitution in Lyp, each in a single patient), suggesting that these phosphatases are infrequently mutated in CLL. The previously reported Lyp polymorphisms R620W and R263Q were observed in 2 additional cases. We next investigated expression of these phosphatases in purified CLL and normal B cells by immunoblotting. Expression of SHP1 and SHP2 was relatively uniform in the different CLL B-cells samples (n=42) and was not different from normal B cells (n=4). In contrast, expression of Lyp was markedly higher in most CLL samples, with 35 of the 49 investigated cases exhibiting 2 to more than 10 fold higher levels than normal B cells (n=5) (CLL, mean Lyp levels 4.7, SD +/−3.7; normal B cells, mean Lyp levels 0.9, SD +/−0.1, P=0.022). The mean Lyp levels were somewhat higher in U-CLL than M-CLL (6.0 vs. 3.9) and ZAP-70-positive than ZAP-70-negative cases (5.6 vs. 4.7), but these differences were not statistically significant. Analysis of Lyp expression in various lymphoma B-cell lines (n=9) also did not reveal significant differences with respect to normal B-cells, suggesting that Lyp overexpression is a specific feature of CLL. To determine what are the consequences of Lyp overexpression on BCR signaling, we downregulated Lyp in primary CLL B-cells by RNA interference and investigated activation of BCR signaling molecules following sIgM crosslinking. Downregulation of Lyp resulted in a substantial increase in BCR-induced phosphorylation of Lyn (Y397), Syk (Y352), BLNK (Y84) and ERK (T202/Y204), suggesting that overexpression of this phosphatase may be at least partially responsible for the lower BCR signaling capacity of CLL B-cells. Since Lyp expression can be induced in resting T cells by activation with anti-CD3, we investigated whether BCR stimulation will have a similar effect on CLL B-cells. A two-fold increase in Lyp levels was observed after 24 hours of sustained BCR stimulation with immobilized anti-IgM, whereas transient stimulation with soluble anti-IgM resulted in a 20% decrease in Lyp levels. These effects were specific for Lyp, since no such changes were observed in the expression of SHP1 and SHP2. In summary, this study shows that CLL B-cells specifically overexpress the phosphatase Lyp, and important negative regulator of BCR signaling that has been implicated in the pathogenesis of several common autoimmune diseases. Given the observation that Lyp can be induced by sustained BCR engagement and in view of recent findings that Lyp is also overexpressed in anergic B cells, these data further support the notion that CLL cells are continuously exposed to (auto)antigen in vivo. Disclosures: No relevant conflicts of interest to declare.


Author(s):  
Oleg Sukmansky

Data, presented in this review, show that gaseous signaling molecules are a common biological system of bioregulators, which attribute to main kingdoms of life – animals, plants and bacteria. They confirm the similarity of their origin and developing by evolution. Gaseous signaling molecules (gasotransmitters) were first discovered and mostly researched in humans and mammals. Today are known gaseous signaling molecules such as: nitric oxide and reactive oxygen species, carbon monoxide, hydrogen sulfide, polysulfides and sulfur dioxide. It is proved that there are more gaseous signaling molecules and more pathways and mechanisms of their production in bacteria than in mammals, so their importance in evolution of living organisms on the planet Earth has decreased. However, in the process of evolution, in connection with the development from simple unicellular organisms into complex, higher multicellular, the number of functional targets that were influenced by gaseous signaling molecules has increased, i.e. their role has been getting increasingly complicated. The endogenous gaseous signaling molecules, produced by bacteria, regulate their metabolism, protect them against antibiotics and promote their colonization in the host organism. So they play an important role in the pathogenesis of infectious diseases in humans and animals. On the other side, the endogenous gaseous signaling molecules of humans and animals have mostly the negative impact on bacteria’s development and increase the host’s resistance to infections. Published data prove the similarity of function and role in pathology of gaseous signaling molecules in invertebrates with those in higher (vertebrate) animals. In particular, this relates to the nervous system and to the role of gaseous signaling molecules in the formation of memory and behavior. The gaseous signaling molecules of non-mammal vertebrata – fishes, amphibians, reptiles, and birds – are especially similar to mammals and humans. Isolated tissues of brain, eyes and lungs of poikilothermic non-mammalian vertebrates (fishes, amphibians and reptiles) are used to study the possible role of gaseous signaling molecules in the pathogenesis of diseases affecting these organs in humans. Further researches of the evolution of gaseous signaling molecules by comparing them in living beings of different levels of development may be useful for exposure of new ways of application in medicine and adjacent fields. The study of their role in the pathogenesis of pathological processes increases the possibilities of treatment and prevention of diseases via utilization of gaseous signaling molecules, their donors, precursors, and inhibitors. Key words: gaseous signaling molecules, evolution, vertebrate, invertebrate, bacteria, biological action, role in pathology. For citation: Sukmansky OI. Gaseous signaling molecules (GSM): evolution, biological role and involvement in the pathogenesis of diseases (literature review). Journal of the National Academy of Medical Sciences of Ukraine. 2019;25(4):373–382


2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Eric DeLeon ◽  
Maaz Arif ◽  
Evelyn Huang ◽  
Yan Gao ◽  
Kenneth Olson

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