The Rice LRR-Like1 Protein YELLOW AND PREMATURE DWARF 1 is Involved in High Light-Induced Leaf Senescence

Abstract Senescence is induced by endogenous physiological changes or exogenous stresses in plants. Here, we isolated two alleles of a novel rice (Oryza sativa L.) mutant, yellow and premature dwarf 1 (ypd1). The ypd1 mutants exhibited a yellow and dwarf phenotype from germination, and premature senescence starting at tillering. Moreover, the ypd1 mutants were sensitive to high light, which accelerated cell death and senescence. Consistent with their yellow phenotype, the ypd1 mutants had abnormal chloroplasts and lower levels of photosynthetic pigments. Trypan blue staining, TUNEL experiments, NBT staining, and DAB staining demonstrated that the ypd1 mutants showed cell death and accumulated reactive oxygen species. Moreover, the ypd1 mutants showed increased expression of senescence-associated genes. Map-based cloning revealed a substitution (G→A) in exon 6 (ypd1-1) and 13 (ypd1-2) of LOC_Os06g13050 that affected splicing and caused premature termination of the encoded protein. YPD1 was preferentially expressed in the leaf and encodes an LRR-Like1 (LRRL1) protein. Complementation, overexpression, and targeted deletion experiments confirmed that the mutations in YPD1 cause the ypd1 phenotype. YPD1 localized on the chloroplast membrane. These findings revealed that the novel rice LRRL1 protein YPD1 affects rice chloroplast development and leaf senescence.

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Regulation of Senescence by Sugar Metabolism

10.32747/2003.7585189.bard ◽

2003 ◽

Author(s):

David Granot ◽

Richard Amasino

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Leaf Senescence ◽

Sugar Metabolism ◽

Regulatory Role ◽

Tomato Plants ◽

Hexokinase Activity ◽

Delayed Senescence ◽

Yeast Genes ◽

Senescence Associated Genes

Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .

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A SUBTILISIN-LIKE SERINE PROTEASE1 (OsSUBSrP1), plays an important role in the wax and cutin pathway, is essential for panicle development in rice

10.1101/2021.07.04.451081 ◽

2021 ◽

Author(s):

Asif Ali ◽

Tingkai Wu ◽

Hongyu Zhang ◽

Peizhou Xu ◽

Syed Adeel Zafar ◽

...

Keyword(s):

Cell Death ◽

Global Gene Expression ◽

Blue Staining ◽

The Novel ◽

Knock Out ◽

Panicle Development ◽

Global Gene Expression Analysis ◽

Normal Meiosis ◽

Spikelet Degeneration

Panicle degeneration is a severe physiological defect and causes reduction in grain yield. In this study, we characterized and presented the functional analysis of our previously reported mutant apa1331 (apical panicle abortion1331) that showed apical spikelet degeneration. The anthers from the apical spikelets of apa1331 were degenerated, pollen-less and showed lack of cuticle formation. Transverse sections showed normal meiosis till stage 5-6, however, defects in post-meiotic microspore development were found at stage 8-9 in apa1331. Measurement of wax and cutin analysis showed a significant reduction in anthers of apa1331 compared to Wildtype (WT). Quantification of H2O2 and MDA has indicated the excessive ROS (reactive oxygen species) in apa1331. Trypan blue staining, and TUNEL assay revealed cell death and excessive DNA fragmentation in apa1331. Map-based cloning and Mutmap analysis identified a candidate gene (LOC_Os04g40720) that is a SUBTILISIN-LIKE SERINE PROTEASE (OsSUBSrP1) which harbored an SNP (A>G) in apa1331. CRISPR-mediated knock-out lines of OsSUBSrP1 displayed spikelet degeneration comparable to apa1331. Global gene expression analysis revealed a significant downregulation of wax and cutin biosynthesis genes e.g., OsWDA1, OsMS2 and OsCER4 in apa1331. Our study reports the novel role of SUBSrP1 in ROS-mediated cell death in panicle development.

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The novel anti-cell death compound MS41 and its cytoprotective mechanism

Neuroscience Research ◽

10.1016/s0168-0102(00)81156-6 ◽

2000 ◽

Vol 38 ◽

pp. S51

Author(s):

R Asakai

Keyword(s):

Cell Death ◽

The Novel

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Programmed cell death during rice leaf senescence is nonapoptotic

New Phytologist ◽

10.1046/j.1469-8137.2002.00443.x ◽

2002 ◽

Vol 155 (1) ◽

pp. 25-32 ◽

Cited By ~ 40

Author(s):

Ruey-Hua Lee ◽

Shu-Chen Grace Chen

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Leaf Senescence ◽

Rice Leaf

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Targeting AKT/mTOR and Bcl-2 for Autophagic and Apoptosis Cell Death in Lung Cancer: Novel Activity of a Polyphenol Compound

Antioxidants ◽

10.3390/antiox10040534 ◽

2021 ◽

Vol 10 (4) ◽

pp. 534

Author(s):

Sucharat Tungsukruthai ◽

Onrapak Reamtong ◽

Sittiruk Roytrakul ◽

Suchada Sukrong ◽

Chanida Vinayanwattikun ◽

...

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cancer Cells ◽

Proteomic Analysis ◽

Interaction Analysis ◽

Time Dependent ◽

The Novel ◽

Protein Protein Interaction ◽

Autophagy Induction ◽

Acidic Vesicle

Autophagic cell death (ACD) is an alternative death mechanism in resistant malignant cancer cells. In this study, we demonstrated how polyphenol stilbene compound PE5 exhibits potent ACD-promoting activity in lung cancer cells that may offer an opportunity for novel cancer treatment. Cell death caused by PE5 was found to be concomitant with dramatic autophagy induction, as indicated by acidic vesicle staining, autophagosome, and the LC3 conversion. We further confirmed that the main death induction caused by PE5 was via ACD, since the co-treatment with an autophagy inhibitor could reverse PE5-mediated cell death. Furthermore, the defined mechanism of action and upstream regulatory signals were identified using proteomic analysis. Time-dependent proteomic analysis showed that PE5 affected 2142 and 1996 proteins after 12 and 24 h of treatment, respectively. The crosstalk network comprising 128 proteins that control apoptosis and 25 proteins involved in autophagy was identified. Protein–protein interaction analysis further indicated that the induction of ACD was via AKT/mTOR and Bcl-2 suppression. Western blot analysis confirmed that the active forms of AKT, mTOR, and Bcl-2 were decreased in PE5-treated cells. Taken together, we demonstrated the novel mechanism of PE5 in shifting autophagy toward cell death induction by targeting AKT/mTOR and Bcl-2 suppression.

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Contrasting roles of GmNAC065 and GmNAC085 in natural senescence, plant development, multiple stresses and cell death responses

Scientific Reports ◽

10.1038/s41598-021-90767-6 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Bruno Paes Melo ◽

Isabela Tristan Lourenço-Tessutti ◽

Otto Teixeira Fraga ◽

Luanna Bezerra Pinheiro ◽

Camila Barrozo de Jesus Lins ◽

...

Keyword(s):

Cell Death ◽

Plant Development ◽

Stress Responses ◽

Regulatory Networks ◽

Lower Stress ◽

Multiple Stresses ◽

Gene Sets ◽

Ros Accumulation ◽

Stress Dependent ◽

Senescence Associated Genes

AbstractNACs are plant-specific transcription factors involved in controlling plant development, stress responses, and senescence. As senescence-associated genes (SAGs), NACs integrate age- and stress-dependent pathways that converge to programmed cell death (PCD). In Arabidopsis, NAC-SAGs belong to well-characterized regulatory networks, poorly understood in soybean. Here, we interrogated the soybean genome and provided a comprehensive analysis of senescence-associated Glycine max (Gm) NACs. To functionally examine GmNAC-SAGs, we selected GmNAC065, a putative ortholog of Arabidopsis ANAC083/VNI2 SAG, and the cell death-promoting GmNAC085, an ANAC072 SAG putative ortholog, for analyses. Expression analysis of GmNAC065 and GmNAC085 in soybean demonstrated (i) these cell death-promoting GmNACs display contrasting expression changes during age- and stress-induced senescence; (ii) they are co-expressed with functionally different gene sets involved in stress and PCD, and (iii) are differentially induced by PCD inducers. Furthermore, we demonstrated GmNAC065 expression delays senescence in Arabidopsis, a phenotype associated with enhanced oxidative performance under multiple stresses, higher chlorophyll, carotenoid and sugar contents, and lower stress-induced PCD compared to wild-type. In contrast, GmNAC085 accelerated stress-induced senescence, causing enhanced chlorophyll loss, ROS accumulation and cell death, decreased antioxidative system expression and activity. Accordingly, GmNAC065 and GmNAC085 targeted functionally contrasting sets of downstream AtSAGs, further indicating that GmNAC85 and GmNAC065 regulators function inversely in developmental and environmental PCD.

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The novel synthesized 2-(3-(methylamino)phenyl)-6-(pyrrolidin-1-yl)quinolin-4-one (Smh-3) compound induces G2/M phase arrest and mitochondrial-dependent apoptotic cell death through inhibition of CDK1 and AKT activity in HL-60 human leukemia cells

International Journal of Oncology ◽

10.3892/ijo.2011.952 ◽

2011 ◽

Vol 38 (5) ◽

Cited By ~ 5

Author(s):

Huang

Keyword(s):

Cell Death ◽

Apoptotic Cell ◽

Apoptotic Cell Death ◽

Leukemia Cells ◽

Human Leukemia ◽

The Novel ◽

Human Leukemia Cells ◽

Phase Arrest ◽

M Phase

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prICE: a downstream target for ceramide-induced apoptosis and for the inhibitory action of Bcl-2

Biochemical Journal ◽

10.1042/bj3160025 ◽

1996 ◽

Vol 316 (1) ◽

pp. 25-28 ◽

Cited By ~ 153

Author(s):

Miriam J. SMYTH ◽

David K. PERRY ◽

Jiandi ZHANG ◽

Guy G. POIRIER ◽

Yusuf A. HANNUN ◽

...

Keyword(s):

Cell Death ◽

Inhibitory Action ◽

Second Messenger ◽

The Novel ◽

Over Expression ◽

Downstream Target ◽

Induced Apoptosis ◽

Insight Into

The novel lipid second messenger, ceramide, specifically induced poly(ADP-ribose) polymerase cleavage through activation of the protease prICE. Over-expression of Bcl-2 inhibited ceramide-induced poly(ADP-ribose) polymerase proteolysis and protected cells from ceramide-induced death. These data provide the first insight into the mechanism by which ceramide mediates apoptosis and suggest a mechanism by which Bcl-2 protects from cell death.

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Ferroptosis-mediated Crosstalk in the Tumor Microenvironment Implicated in Cancer Progression and Therapy

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.739392 ◽

2021 ◽

Vol 9 ◽

Author(s):

Yini Liu ◽

Chunyan Duan ◽

Rongyang Dai ◽

Yi Zeng

Keyword(s):

Cell Death ◽

Tumor Microenvironment ◽

Cancer Progression ◽

Cancer Biology ◽

Lipid Peroxides ◽

Antioxidant Systems ◽

Biological Processes ◽

The Novel ◽

Regulated Cell Death ◽

Novel Therapeutic Strategies

Ferroptosis is a recently recognized form of non-apoptotic regulated cell death and usually driven by iron-dependent lipid peroxidation and has arisen to play a significant role in cancer biology. Distinct from other types of cell death in morphology, genetics, and biochemistry, ferroptosis is characterized by the accumulation of lipid peroxides and lethal reactive oxygen species controlled by integrated oxidant and antioxidant systems. Increasing evidence indicates that a variety of biological processes, including amino acid, iron, lactate, and lipid metabolism, as well as glutathione, phospholipids, NADPH, and coenzyme Q10 biosynthesis, are closely related to ferroptosis sensitivity. Abnormal ferroptotic response may modulate cancer progression by reprogramming the tumor microenvironment (TME). The TME is widely associated with tumor occurrence because it is the carrier of tumor cells, which interacts with surrounding cells through the circulatory and the lymphatic system, thus influencing the development and progression of cancer. Furthermore, the metabolism processes play roles in maintaining the homeostasis and evolution of the TME. Here, this review focuses on the ferroptosis-mediated crosstalk in the TME, as well as discussing the novel therapeutic strategies for cancer treatment.

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