scholarly journals Phenylalanine Suppresses Cell Death Caused by Loss of Fumarylacetoacetate Hydrolase in Arabidopsis

2022 ◽  
Author(s):  
Yihe Jiang ◽  
Qi Zhu ◽  
Hua Yang ◽  
Tiantian Zhi ◽  
Chunmei Ren
Keyword(s):  
Cell Death ◽  
Methyl Jasmonate ◽  
Chlorophyll Biosynthesis ◽  
Phenylpropanoid Pathway ◽  
Degradation Pathway ◽  
Marker Genes ◽  
Jasmonate Signaling ◽  
Short Day ◽  
Fumarylacetoacetate Hydrolase

Abstract Fumarylacetoacetate hydrolase (FAH) catalyzes the final step of Tyrosine (Tyr) degradation pathway essential to animals and the deficiency of FAH causes an inborn lethal disease. In plants, a role of this pathway was unknown until we found that mutation of Short-day Sensitive Cell Death1 (SSCD1), encoding Arabidopsis FAH, results in cell death under short day. Phenylalanine (Phe) could be converted to Tyr and then degraded in both animals and plants. Phe ingestion in animals worsens the disease caused by FAH defect. However, in this study we found that Phe represses cell death caused by FAH defect in plants. Phe treatment promoted chlorophyll biosynthesis and suppressed the up‑regulation of reactive oxygen species marker genes in the sscd1 mutant. Furthermore, the repression of sscd1 cell death by Phe could be reduced by α-aminooxi-β-phenylpropionic acid but increased by methyl jasmonate, which inhibits or activates Phe ammonia-lyase catalyzing the first step of phenylpropanoid pathway, respectively. In addition, we found that jasmonate signaling up‑regulates Phe ammonia-lyase 1 and mediates the methyl jasmonate enhanced repression of sscd1 cell death by Phe. These results uncovered the relation between chlorophyll biosynthesis, phenylpropanoid pathway and jasmonate signaling in regulating the cell death resulting from loss of FAH in plants.

Exogenous application of methyl jasmonate induces defense response and develops tolerance against mungbean yellow mosaic India virus in Vigna mungo

2019 ◽  
Vol 46 (1) ◽  
pp. 69 ◽  
Author(s):  
Nibedita Chakraborty ◽  
Jolly Basak
Keyword(s):  
Methyl Jasmonate ◽  
Molecular Mechanisms ◽  
Stability Index ◽  
Protective Role ◽  
Membrane Stability ◽  
Vigna Mungo ◽  
Marker Genes ◽  
Exogenous Application ◽  
Ros Homeostasis

Vigna mungo (L.)Hepper is an economically important leguminous crop in south-east Asia. However, its production is severely affected by Mungbean yellow mosaic India virus (MYMIV). It is well established that methyl jasmonate (MeJA) is effective in inducing resistance against pathogens in several plants. To assess the role of MeJA in developing MYMIV tolerance in V. mungo, we analysed time-dependent biochemical and molecular responses of MYMIV susceptible V. mungo after exogenous application of different MeJA concentrations, followed by MYMIV infection. Our analysis revealed that exogenous application of different concentrations of MeJA resulted in decreased levels of malondialdehyde with higher membrane stability index values in MYMIV susceptible V. mungo, suggesting the protective role of MeJA through restoring the membrane stability. Moreover, the level of expression of different antioxidative enzymes revealed that exogenous MeJA is also very effective in ROS homeostasis maintenance. Enhanced expressions of the defence marker genes lipoxygenase and phenylalanine ammonia-lyase and the reduced expression of the MYMIV coat-protein encoding gene in all MeJA treated plants post MYMIV infection revealed that exogenous application of MeJA is effective for MYMIV tolerance in V. mungo. Our findings provide new insights into the physiological and molecular mechanisms of MYMIV tolerance in Vigna induced by MeJA.

scholarly journals Root-derived trans-zeatin cytokinin protects Arabidopsis plants against photoperiod stress

2020 ◽  
Author(s):  
Manuel Frank ◽  
Anne Cortleven ◽  
Ondrej Novak ◽  
Thomas Schmülling
Keyword(s):  
Cell Death ◽  
Response Regulator ◽  
Light Period ◽  
Negative Regulator ◽  
Marker Genes ◽  
Signaling Proteins ◽  
Negative Consequences ◽  
Regulatory Circuit ◽  
Cytokinin Synthesis

ABSTRACTRecently, a novel type of abiotic stress caused by a prolongation of the light period - coined photoperiod stress - has been described in Arabidopsis. During the night after the prolongation of the light period, stress and cell death marker genes are induced. The next day, strongly stressed plants display a reduced photosynthetic efficiency and leaf cells eventually enter programmed cell death. The phytohormone cytokinin (CK) acts as a negative regulator of this photoperiod stress syndrome. In this study, we show that Arabidopsis wild-type plants increase the CK concentration in response to photoperiod stress. Analysis of cytokinin synthesis and transport mutants revealed that root-derived trans-zeatin (tZ)-type CKs protect against photoperiod stress. The CK signaling proteins ARABIDOPSIS HISTIDINE PHOSPHOTRANSFER PROTEIN 2 (AHP2), AHP3 and AHP5 and transcription factors ARABIDOPSIS RESPONSE REGULATOR 2 (ARR2), ARR10 and ARR12 are required for the protective activity of CK. Analysis of higher order B-type arr mutants suggested that a complex regulatory circuit exists in which the loss of ARR10 or ARR12 can rescue the arr2 phenotype. Together the results revealed the role of root-derived CK acting in the shoot through the two-component signaling system to protect from the negative consequences of strong photoperiod stress.

scholarly journals Disruption of Fumarylacetoacetate Hydrolase Causes Spontaneous Cell Death under Short-Day Conditions in Arabidopsis

2013 ◽  
Vol 162 (4) ◽  
pp. 1956-1964 ◽  
Author(s):  
Chengyun Han ◽  
Chunmei Ren ◽  
Tiantian Zhi ◽  
Zhou Zhou ◽  
Yan Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Short Day ◽  
Fumarylacetoacetate Hydrolase ◽  
Spontaneous Cell Death

scholarly journals DUAL ROLE OF AUTOPHAGY IN PERIODONTAL DISEASE

2021 ◽  
Vol 5 (6) ◽  
Author(s):  
Priyanka Muwal ◽  
Navneet Kaur ◽  
Gurpreet Kaur
Keyword(s):  
Cell Death ◽  
Periodontal Disease ◽  
Cell Function ◽  
Apoptotic Cell ◽  
Degradation Pathway ◽  
Oral Disease ◽  
Periodontal Pathogens ◽  
Evolutionarily Conserved ◽  
Novel Host

Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress.  The induction of autophagy has been shown to have both protective and pathological effects in periodontitis. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy is an evolutionarily conserved process essential for cellular homeostasis and human health. Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. It also participates in various biological processes, such as cellular differentiation, cell function, and defense against pathogens. In addition, autophagic dysfunction is associated with multiple diseases such as autoimmune disease, cancer, diabetes, and oral disease.  Nowadays research has ascertained the role of autophagy in Periodontal disease, especially its role in the host defence against periodontal disease drivers. A bulk of research has recognized several pharmaceuticals and nutraceuticals that can potentially modulate this kind of cell death and serve as useful therapies. However, further research is warranted in order to reach a clinical translation, which could be of help in the discovery of novel host modulation therapies for Periodontal disease. Keywords: Autophagy, Apoptosis, Micro autophagy, immune response, Periodontitis, Periodontal pathogens, Periapical lesion

The role of programmed cell death ligand-1/ programmed cell death-1 (PD-L1/PD-1) in HPV-induced cervical cancer and potential for their use in blockade therapy

2020 ◽  
Vol 27 ◽  
Author(s):  
Lifang Zhang ◽  
Yu Zhao ◽  
Quanmei Tu ◽  
Xiangyang Xue ◽  
Xueqiong Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Escape ◽  
Hypoxia Inducible Factor ◽  
Hpv Infection ◽  
Advanced Cervical Cancer ◽  
Cervical Carcinogenesis ◽  
Programmed Cell Death 1

Background: Cervical cancer induced by infection with human papillomavirus (HPV) remains a leading cause of mortality for women worldwide although preventive vaccines and early diagnosis have reduced morbidity and mortality. Advanced cervical cancer can only be treated with either chemotherapy or radiotherapy but outcomes are poor. The median survival for advanced cervical cancer patients is only 16.8 months. Methods: We undertook a structural search of peer-reviewed published studies based on 1). Characteristics of programmed cell death ligand-1/programmed cell death-1(PD-L1/PD-1) expression in cervical cancer and upstream regulatory signals of PD-L1/PD-1 expression, 2). The role of the PD-L1/PD-1 axis in cervical carcinogenesis induced by HPV infection and 3). Whether the PD-L1/PD-1 axis has emerged as a potential target for cervical cancer therapies. Results: One hundred and twenty-six published papers were included in the review, demonstrating that expression of PD-L1/PD-1 is associated with HPV-caused cancer, especially with HPV 16 and 18 which account for approximately 70% of cervical cancer cases. HPV E5/E6/E7 oncogenes activate multiple signaling pathways including PI3K/AKT, MAPK, hypoxia-inducible factor 1α, STAT3/NF-kB and MicroRNAs, which regulate PD-L1/PD-1 axis to promote HPV-induced cervical carcinogenesis. The PD-L1/PD-1 axis plays a crucial role in immune escape of cervical cancer through inhibition of host immune response. creating an "immune-privileged" site for initial viral infection and subsequent adaptive immune resistance, which provides a rationale for therapeutic blockade of this axis in HPV-positive cancers. Currently, Phase I/II clinical trials evaluating the effects of PD-L1/PD-1 targeted therapies are in progress for cervical carcinoma, which provide an important opportunity for the application of anti-PD-L1/anti-PD-1 antibodies in cervical cancer treatment. Conclusion: Recent research developments have led to an entirely new class of drugs using antibodies against the PD-L1/PD-1 thus promoting the body’s immune system to fight the cancer. The expression and roles of the PD-L1/ PD-1 axis in the progression of cervical cancer provide great potential for using PD-L1/PD-1 antibodies as a targeted cancer therapy.

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