Ectopic expression of peanut acyl carrier protein in tobacco alters fatty acid composition in the leaf and resistance to cold stress

Tang, Guiying; Wei, Lijuan; Liu, Z. J.; Bi, Ye; Shan, Lei

doi:10.1007/s10535-012-0057-7

Cited by 25 publications

(26 citation statements)

References 28 publications

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“…[121][122][123] A number of chemotherapy drugs exert stress on the cancer genome, most of which act as genotoxicants that damage the DNA and induce the DDR; these include DNA cross-linkers, topoisomerase poisons, and alkylating agents. [124][125][126] Although conventional anticancer agents were developed to selectively target highly proliferative cancer cells over normal cells, highly proliferative normal tissues (e.g. bone marrow, gut epithelium) are also targeted, and the side effects can sometimes be life-threatening.…”

Section: Genotoxic Stressmentioning

confidence: 99%

Therapeutic targeting of cellular stress responses in cancer

Chen

Xie

2018

Thoracic Cancer

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Similar to bacteria, yeast, and other organisms that have evolved pathways to respond to environmental stresses, cancer cells develop mechanisms that increase genetic diversity to facilitate adaptation to a variety of stressful conditions, including hypoxia, nutrient deprivation, exposure to DNA‐damaging agents, and immune responses. To survive, cancer cells trigger mechanisms that drive genomic instability and mutation, alter gene expression programs, and reprogram the metabolic pathways to evade growth inhibition signaling and immune surveillance. A deeper understanding of the molecular mechanisms that underlie the pathways used by cancer cells to overcome stresses will allow us to develop more efficacious strategies for cancer therapy. Herein, we overview several key stresses imposed on cancer cells, including oxidative, metabolic, mechanical, and genotoxic, and discuss the mechanisms that drive cancer cell responses. The therapeutic implications of these responses are also considered, as these factors pave the way for the targeting of stress adaption pathways in order to slow cancer progression and block resistance to therapy.

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Section: Genotoxic Stressmentioning

confidence: 99%

Therapeutic targeting of cellular stress responses in cancer

Chen

Xie

2018

Thoracic Cancer

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“…Recent studies have shown that the light signaling gene phyB also participates in a pathway that promotes resistance to chilling . PhyB negatively regulates chloroplast structural stability by lowering levels of unsaturated fatty acids present in membrane lipids . PhyB deficiency positively regulates OsPIL16 and OsDREB1 , thereby alleviating chilling‐induced photoinhibition and enhancing chilling tolerance .…”

Section: Temperature Changesmentioning

confidence: 99%

“…[135][136][137] PhyB negatively regulates chloroplast structural stability by lowering levels of unsaturated fatty acids present in membrane lipids. [138][139][140] PhyB deficiency positively regulates OsPIL16 and OsDREB1, 141 thereby alleviating chilling-induced photoinhibition and enhancing chilling tolerance. [142][143][144] Similar mechanisms have also been characterized in Suaeda salsa.…”

Section: Salt Stressmentioning

confidence: 99%

Molecular mechanisms underlying stress response and adaptation

Sun

Zhou

2017

Thoracic Cancer

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Environmental stresses are ubiquitous and unavoidable to all living things. Organisms respond and adapt to stresses through defined regulatory mechanisms that drive changes in gene expression, organismal morphology, or physiology. Immune responses illustrate adaptation to bacterial and viral biotic stresses in animals. Dysregulation of the genotoxic stress response system is frequently associated with various types of human cancer. With respect to plants, especially halophytes, complicated systems have been developed to allow for plant growth in high salt environments. In addition, drought, waterlogging, and low temperatures represent other common plant stresses. In this review, we summarize representative examples of organismal response and adaptation to various stresses. We also discuss the molecular mechanisms underlying the above phenomena with a focus on the improvement of organismal tolerance to unfavorable environments.

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“…Plants can detect various environmental signals such as high salt concentration (Shen et al, 2014;Wang S. et al, 2014;Sui et al, 2017), cold temperature (Tang et al, 2012;Liu et al, 2013;Zhao X. et al, 2014;, reactive oxygen species levels (Li K. et al, 2012), waterlogging (Song et al, 2011;Chen et al, 2016;, phosphate scarcity , and ultraviolet (UV) radiation Deng et al, 2015). Failure to appropriately respond to these stressors decreases plant productivity and affects human food and animal feed supplies.…”

Section: Introductionmentioning

confidence: 99%

Cell Cycle Regulation in the Plant Response to Stress

2020

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As sessile organisms, plants face a variety of environmental challenges. Their reproduction and survival depend on their ability to adapt to these stressors, which include water, heat stress, high salinity, and pathogen infection. Failure to adapt to these stressors results in programmed cell death and decreased viability, as well as reduced productivity in the case of crop plants. The growth and development of plants are maintained by meiosis and mitosis as well as endoreduplication, during which DNA replicates without cytokinesis, leading to polyploidy. As in other eukaryotes, the cell cycle in plants consists of four stages (G1, S, G2, and M) with two major check points, namely, the G1/S check point and G2/M check point, that ensure normal cell division. Progression through these checkpoints involves the activity of cyclin-dependent kinases and their regulatory subunits known as cyclins. In order for plants to survive, cell cycle control must be balanced with adaption to dynamic environmental conditions. In this review, we summarize recent advances in our understanding of cell cycle regulation in plants, with a focus on the molecular interactions of cell cycle machinery in the context of stress tolerance. FIGURE 1 | Schematic representation of the mitotic cell cycle in plants.At the G1 phase, D-type cyclins (CYCD) interact with the A-type CDK (CDKA), forming the CDKA/CYCD complex. The activity of CDKA/CYCD complex can be negatively regulated by KPR and SIM proteins. Once activation, this complex phosphorylates RBR to release the transcript factor E2Fa/b-DP. This E2Fa/b-DP complex binds to the E2F box and activate the transcription of S phase genes. At the G2 and M phase S, CYCA and CYCB are strongly expressed and their gene products assemble with CDKA and CDKB. The CYCD can also associate with CDKs. At the beginning of G2 phase, CDK activity are inhibited because of the phosphorylation of Y14 and T15 site by WEEI kinase. The CDC25-related kinase, which removes the inhibitory phosphate groups, still needs to be identified. Once the CDK/CYC complex are active, they phosphorylate MYB3R transcription factors and activate mitotic genes' transcription. Mitotic exit requires anaphase-promoting complex (APC), which degrades cyclins through ubiquitin-proteasome pathway.

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Ectopic expression of peanut acyl carrier protein in tobacco alters fatty acid composition in the leaf and resistance to cold stress

Cited by 25 publications

References 28 publications

Therapeutic targeting of cellular stress responses in cancer

Therapeutic targeting of cellular stress responses in cancer

Molecular mechanisms underlying stress response and adaptation

Cell Cycle Regulation in the Plant Response to Stress

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