scholarly journals Signaling pathways in the coral polyp bail-out response

Coral Reefs ◽  
2020 ◽  
Vol 39 (6) ◽  
pp. 1535-1548
Author(s):  
Po-Shun Chuang ◽  
Satoshi Mitarai

AbstractPolyp bail-out is a stress response exhibited by some pocilloporid corals, with mechanisms and consequences distinct from those of bleaching. Although induction of polyp bail-out has been demonstrated in the laboratory, molecular mechanisms underlying this response have rarely been discussed. We conducted genetic analyses of Pocillopora acuta during initiation of hyperosmosis-induced polyp bail-out, using both transcriptomic and qPCR techniques. Beyond upregulation of apoptosis and proteolysis, corals showed significant activation of tumor necrosis factor and fibroblast growth factor (FGF) signaling pathways during induction of polyp bail-out. In our qPCR analysis, a common upregulation profile, peaking at 43.0‰ salinity, was found in the FAS and CASP8 genes, whereas a different profile, showing significant upregulation up to 45.0‰, was displayed by matrix metalloproteinases and genes in the FGF signaling pathway. These results suggest parallel involvement of an extrinsic apoptotic signaling pathway and FGF-mediated extracellular matrix degradation in polyp bail-out. Furthermore, in the XIAP, JNK, and NFKB1 genes, we detected a third expression profile showing linear upregulation that becomes maximal at the endpoint salinity level of the experiment (46.0‰), indicating activation of anti-apoptotic and cell survival signals during polyp bail-out. Our results provide new insights into signaling pathways responsible for polyp bail-out and suggest the feasibility of inducing bail-out by specifically triggering these pathways without exerting lethal stresses on the corals, which in turn will facilitate acquisition of viable polyps for possible use in coral reef restoration.

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jingfang Dong ◽  
Lian Zhou ◽  
Aiqing Feng ◽  
Shaohong Zhang ◽  
Hua Fu ◽  
...  

Abstract Background Although panicle blast is more destructive to yield loss than leaf blast in rice, the cloned genes that function in panicle blast resistance are still very limited and the molecular mechanisms underlying panicle blast resistance remain largely unknown. Results In the present study, we have confirmed that the three Oxalate oxidase (OXO) genes, OsOXO2, OsOXO3 and OsOXO4 from a blast-resistant cultivar BC10 function in panicle blast resistance in rice. The expression of OsOXO2, OsOXO3 and OsOXO4 were induced by panicle blast inoculation. Subcellular localization analysis revealed that the three OXO proteins are all localized in the nucleus and cytoplasm. Simultaneous silencing of OsOXO2, OsOXO3 and OsOXO4 decreased rice resistance to panicle blast, whereas the OsOXO2, OsOXO3 and OsOXO4 overexpression rice plants individually showed enhanced panicle blast resistance. More H2O2 and higher expression levels of PR genes were observed in the overexpressing plants than in the control plants, while the silencing plants exhibited less H2O2 and lower expression levels of PR genes compared to the control plants. Moreover, phytohormone treatment and the phytohormone signaling related gene expression analysis showed that panicle blast resistance mediated by the three OXO genes was associated with the activation of JA and ABA signaling pathways but suppression of SA signaling pathway. Conclusion OsOXO2, OsOXO3 and OsOXO4 positively regulate panicle blast resistance in rice. The OXO genes could modulate the accumulation of H2O2 and expression levels of PR gene in plants. Moreover, the OXO genes mediated panicle blast resistance could be regulated by ABA, SA and JA, and may be associated with the activation of JA and ABA signaling pathways but suppression of the SA signaling pathway.


2018 ◽  
Vol 19 (8) ◽  
pp. 2201 ◽  
Author(s):  
Ke Li ◽  
Yongqi Liang ◽  
Libo Xing ◽  
Jiangping Mao ◽  
Zhen Liu ◽  
...  

Adventitious roots (AR) play an important role in the vegetative propagation of apple rootstocks. The potential role of hormone, wounding, and sugar signalling pathways in mediating AR formation has not been adequately explored and the whole co-expression network in AR formation has not been well established in apple. In order to identify the molecular mechanisms underlying AR formation in ‘T337’ apple rootstocks, transcriptomic changes that occur during four stages of AR formation (0, 3, 9 and 16 days) were analyzed using high-throughput sequencing. A total of 4294 differentially expressed genes were identified. Approximately 446 genes related to hormones, wounding, sugar signaling, root development, and cell cycle induction pathways were subsequently selected based on their potential to be involved in AR formation. RT-qPCR validation of 47 genes with known functions exhibited a strong positive correlation with the RNA-seq data. Interestingly, most of the candidate genes involved in AR formation that were identified by transcriptomic sequencing showed auxin-responsive expression patterns in an exogenous Indole-3-butyric acid (IBA)-treatment assay: Indicating that endogenous and exogenous auxin plays key roles in regulating AR formation via similar signalling pathways to some extent. In general, AR formation in apple rootstocks is a complex biological process which is mainly influenced by the auxin signaling pathway. In addition, multiple hormones-, wounding- and sugar-signaling pathways interact with the auxin signaling pathway and mediate AR formation in apple rootstocks.


2011 ◽  
Vol 236 (11) ◽  
pp. 1306-1313 ◽  
Author(s):  
Ji-Hyun Park ◽  
Yoon-Seup Kum ◽  
Tae-Im Lee ◽  
Soo-Jung Kim ◽  
Woo-Ram Lee ◽  
...  

Liver fibrosis represents a process of healing and scarring in response to chronic liver injury. Following injury, an acute inflammation response takes place resulting in moderate cell necrosis and extracellular matrix damage. Melittin, the major bioactive component in the venom of honey bee Apis mellifera, is a 26-residue amphipathic peptide with well-known cytolytic, antimicrobial and proinflammatory properties. However, the molecular mechanisms responsible for the anti-inflammatory activity of melittin have not been elucidated in liver fibrosis. We investigated whether melittin ameliorates liver inflammation and fibrosis in thioacetamide (TAA)-induced liver fibrosis. Two groups of mice were treated with TAA (200 mg/L, in drinking water), one of the groups of mice was co-treated with melittin (0.1 mg/kg) for 12 weeks while the other was not. Hepatic stellate cells (HSCs) were cultured with tumor necrosis factor α in the absence or presence of melittin. Melittin suppresses the expression of proinflammatory cytokines through the nuclear factor (NF)- κB signaling pathway. Moreover, melittin reduces the activity of HSCs in vitro, and decreases the expression of fibrotic gene responses in TAA-induced liver fibrosis. Taken together, melittin prevents TAA-induced liver fibrosis by inhibiting liver inflammation and fibrosis, the mechanism of which is the interruption of the NF- κB signaling pathway. These results suggest that melittin could be an effective agent for preventing liver fibrosis.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jianxing Zeng ◽  
Yingying Jing ◽  
Qionglan Wu ◽  
Jinhua Zeng ◽  
Lixin Wei ◽  
...  

The molecular mechanisms regulating differentiation of hepatic progenitor cells (HPCs), which play pivotal roles in liver regeneration and development, remain obscure. Autophagy and Wnt signaling pathways regulate the development and differentiation of stem cells in various organs. However, the roles of autophagy and Wnt signaling pathways in hepatic differentiation of HPCs are not well understood. Here, we describe the effects of autophagy and Wnt signaling pathways during hepatic differentiation of HPCs. We used a well-established rat hepatic progenitor cell line called WB-F344, which was treated with differentiation medium to promote differentiation of WB-F344 cells along the hepatic phenotype. Firstly, autophagy was highly activated in HPCs and gradually decreased during hepatic differentiation of HPCs. Induction of autophagy by rapamycin or starvation suppressed hepatic differentiation of HPCs. Secondly, Wnt3a signaling pathway was downregulated, and Wnt5a signaling pathway was upregulated in hepatic differentiation of HPCs. At last, Wnt3a signaling pathway was enhanced, and Wnt5a signaling pathway was inhibited by activation of autophagy during hepatic differentiation of HPCs. In summary, these results demonstrate that autophagy regulates hepatic differentiation of hepatic progenitor cells through Wnt signaling pathway.


2014 ◽  
Vol 53 (1) ◽  
pp. R21-R37 ◽  
Author(s):  
Zhen-Yu She ◽  
Wan-Xi Yang

Sex determination refers to the developmental decision that directs the bipotential genital ridge to develop as a testis or an ovary. Genetic studies on mice and humans have led to crucial advances in understanding the molecular fundamentals of sex determination and the mutually antagonistic signaling pathway. In this review, we summarize the current molecular mechanisms of sex determination by focusing on the known critical sex determining genes and their related signaling pathways in mammalian vertebrates from mice to humans. We also discuss the underlying delicate balance between testis and ovary sex determination pathways, concentrating on the antagonisms between major sex determining genes.


BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Razgar Seyed Rahmani ◽  
Tao Shi ◽  
Dongzhi Zhang ◽  
Xiaoping Gou ◽  
Jing Yi ◽  
...  

Abstract Background Brassinosteroid (BR) signaling regulates plant growth and development in concert with other signaling pathways. Although many genes have been identified that play a role in BR signaling, the biological and functional consequences of disrupting those key BR genes still require detailed investigation. Results Here we performed phenotypic and transcriptomic comparisons of A. thaliana lines carrying a loss-of-function mutation in BRI1 gene, bri1–5, that exhibits a dwarf phenotype and its three activation-tag suppressor lines that were able to partially revert the bri1–5 mutant phenotype to a WS2 phenotype, namely bri1–5/bri1–1D, bri1–5/brs1–1D, and bri1–5/bak1–1D. From the three investigated bri1–5 suppressors, bri1–5/bak1–1D was the most effective suppressor at the transcriptional level. All three bri1–5 suppressors showed altered expression of the genes in the abscisic acid (ABA signaling) pathway, indicating that ABA likely contributes to the partial recovery of the wild-type phenotype in these bri1–5 suppressors. Network analysis revealed crosstalk between BR and other phytohormone signaling pathways, suggesting that interference with one hormone signaling pathway affects other hormone signaling pathways. In addition, differential expression analysis suggested the existence of a strong negative feedback from BR signaling on BR biosynthesis and also predicted that BRS1, rather than being directly involved in signaling, might be responsible for providing an optimal environment for the interaction between BRI1 and its ligand. Conclusions Our study provides insights into the molecular mechanisms and functions of key brassinosteroid (BR) signaling genes, especially BRS1.


2020 ◽  
Author(s):  
Jingfang Dong ◽  
Lian Zhou ◽  
Aiqing Feng ◽  
Shaohong Zhang ◽  
Hua Fu ◽  
...  

Abstract Background Although panicle blast is more destructive to yield loss than leaf blast in rice, the cloned genes that function in panicle blast resistance is still very limited and the molecular mechanisms underlying panicle blast resistance remain largely unknown. Results In the present study, we have confirmed that the three OXO genes, OsOXO2, OsOXO3 and OsOXO4 from a blast-resistant cultivar BC10 function in panicle blast resistance in rice. The expression of OsOXO2, OsOXO3 and OsOXO4 were induced by panicle blast inoculation. Subcellular localization analysis revealed that the three OXO genes are all localized in the cell wall. Simultaneous silencing of OsOXO2, OsOXO3 and OsOXO4 decreased rice resistance to panicle blast, whereas the OsOXO2, OsOXO3 and OsOXO4 overexpression rice plants showed enhanced panicle blast resistance. More H2O2 and higher expression levels of PR genes were observed in the overexpressing plants than in the control plants, while the gene silencing plants exhibited less H2O2 and lower expression levels of PR genes compared to the control plants. Moreover, phytohormone treatment and the gene expression analysis showed that panicle blast resistance mediated by the three OXO genes was associated with the induction of JA and ABA signaling pathways but suppression of SA signaling pathway. Conclusion OsOXO2, OsOXO3 and OsOXO4 positively regulate panicle blast resistance in rice. The OXO genes could modulate the accumulation of H2O2 and expression levels of PR gene in plants. Moreover, the OXO genes mediated panicle blast resistance is associated with the activation of JA and ABA signaling pathways but suppression of the SA signaling pathway.


2020 ◽  
Author(s):  
Razgar Seyed Rahmani ◽  
Tao Shi ◽  
Dongzhi Zhang ◽  
Xiaoping Gou ◽  
Jing Yi ◽  
...  

Abstract BackgroundBrassinosteroid (BR) signaling regulates plant growth and development in concert with other signaling pathways. Although many genes have been identified that play a role in Brassinosteroid (BR) signaling, the biological and functional consequences of disrupting those key BR genes still requires detailed investigation.ResultsHere we performed phenotypic and transcriptomic comparisons of A. thaliana lines carrying a loss-of-function mutation in BRI1 gene, bri1-5, that exhibits a dwarf phenotype along with its three activation-tag suppressor lines that were able to partially revert the bri1-5 mutant phenotype to a WT phenotype, namely bri1-5/bri1-1D, bri1-5/brs1-1D, bri1-5/bak1-1D. From the three investigated bri1-5 suppressors, bri1-5/bak1-1D was the most effective suppressor at the transcriptional level. All three bri1-5 suppressors showed altered expression of the genes in the abscisic acid (ABA signaling) pathway, indicating that ABA likely contributes to the partial recovery of the wild type phenotype in these bri1-5 suppressors. Network analysis revealed crosstalk between BR and other phytohormone signaling pathways, suggesting that interference with one hormone signaling pathway affects other hormone signaling pathways. In addition, differential expression analysis suggested the existence of a strong negative feedback from BR signaling on BR biosynthesis and also predicted that BRS1, rather than being directly involved in signaling, is likely responsible for providing an optimal environment for the interaction between BRI1 and its ligand. ConclusionsOur study provides insights into the molecular mechanisms and functions of key brassinosteroid (BR) signaling genes, especially BRS1.


Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 491 ◽  
Author(s):  
Manali Dimri ◽  
Ande Satyanarayana

Hepatocellular carcinoma (HCC) is a complex biological process and is often diagnosed at advanced stages with no effective treatment options. With advances in tumor biology and molecular genetic profiling, several different signaling pathways and molecular mechanisms have been identified as responsible for initiating and promoting HCC. Targeting these critical pathways, which include the receptor tyrosine kinase pathways, the Ras mitogen-activated protein kinase (Ras/Raf/MAPK), the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR), the Wnt/β-catenin signaling pathway, the ubiquitin/proteasome degradation and the hedgehog signaling pathway has led to the identification of novel therapeutics for HCC treatment. In this review, we elaborated on our current understanding of the signaling pathways involved in the development and initiation of HCC and anticipate the potential targets for therapeutic drug development.


Author(s):  
Wen Xu ◽  
Bei Wang ◽  
Yisong Gao ◽  
Yuxuan Cai ◽  
Jiali Zhang ◽  
...  

: Alkaloids are nitrogen-containing organic compounds widely found in natural products, which play an essential role in clinical treatment. Cellular signaling pathways in tumors are a series of enzymatic reaction pathways that convert extracellular signals into intracellular signals to produce biological effects. The ordered function of cell signaling pathways is essential for tumor cell proliferation, differentiation, and programmed death. This review describes the antitumor progression mediated by various alkaloids after inhibiting classical signaling pathways; related studies are systematically retrieved and collected through PubMed. We selected the four currently most popular pathways for discussion and introduced the molecular mechanisms mediated by alkaloids in different signaling pathways, including the NF-kB signaling pathway, PI3K/AKT signaling pathway, MAPK signaling pathway, and P53 signaling pathway. The research progress of alkaloids related to tumor signal transduction pathways and the realization of alkaloids as cancer prevention drugs by targeting signal pathways remains.


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