scholarly journals Priming with a Seaweed Extract Strongly Improves Drought Tolerance in Arabidopsis

2021 ◽  
Vol 22 (3) ◽  
pp. 1469
Author(s):  
Fiaz Rasul ◽  
Saurabh Gupta ◽  
Justyna Jadwiga Olas ◽  
Tsanko Gechev ◽  
Neerakkal Sujeeth ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Drought Stress ◽  
Plant Growth ◽  
Cell Cycle Progression ◽  
Cell Damage ◽  
Marker Gene ◽  
Future Research ◽  
Ion Leakage ◽  
Natural Ecosystems ◽  
Meristem Cell

Drought represents a major threat to plants in natural ecosystems and agricultural settings. The biostimulant Super Fifty (SF), produced from the brown alga Ascophyllum nodosum, enables ecologically friendly stress mitigation. We investigated the physiological and whole-genome transcriptome responses of Arabidopsis thaliana to drought stress after a treatment with SF. SF strongly decreased drought-induced damage. Accumulation of reactive oxygen species (ROS), which typically stifle plant growth during drought, was reduced in SF-primed plants. Relative water content remained high in SF-treated plants, whilst ion leakage, a measure of cell damage, was reduced compared to controls. Plant growth requires a functional shoot apical meristem (SAM). Expression of a stress-responsive negative growth regulator, RESPONSIVE TO DESICCATION 26 (RD26), was repressed by SF treatment at the SAM, consistent with the model that SF priming maintains the function of the SAM during drought stress. Accordingly, expression of the cell cycle marker gene HISTONE H4 (HIS4) was maintained at the SAMs of SF-primed plants, revealing active cell cycle progression after SF priming during drought. In accordance with this, CYCP2;1, which promotes meristem cell division, was repressed by drought but enhanced by SF. SF also positively affected stomatal behavior to support the tolerance to drought stress. Collectively, our data show that SF priming mitigates multiple cellular processes that otherwise impair plant growth under drought stress, thereby providing a knowledge basis for future research on crops.

scholarly journals Phytosulfokine-.ALPHA., a Peptidyl Plant Growth Factor, Stimulates Cell Cycle Progression in Carrot Non-Embryogenic Cells.

2003 ◽  
Vol 20 (3) ◽  
pp. 195-205 ◽  
Author(s):  
Chang-Ho EUN ◽  
Suk-Min KO ◽  
Katsumi HIGASHI ◽  
Dennis YEO ◽  
Yoshikatsu MATSUBAYASHI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Plant Growth ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Embryogenic Cells

Modulation of cell cycle progression and chromatin dynamic as tolerance mechanisms to salinity and drought stress in maize

2020 ◽  
Author(s):  
Khaled Y. Kamal ◽  
Mortaza Khodaeiaminjan ◽  
Galal Yahya ◽  
Ahmed A. El‐Tantawy ◽  
Diaa Abdel El‐Moneim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Drought Stress ◽  
Cell Cycle Progression ◽  
Tolerance Mechanisms ◽  
Cycle Progression ◽  
Chromatin Dynamic

scholarly journals Opposite Effects of the Triple Target (DNA-PK/PI3K/mTOR) Inhibitor PI-103 on the Radiation Sensitivity of Glioblastoma Cell Lines MO59K and MO59J Differing in DNA-PK and ATM Status

2020 ◽  
Author(s):  
Cholpon S. Djuzenova ◽  
Thomas Fischer ◽  
Astrid Katzer ◽  
Dmitri Sisario ◽  
Tessa Korsa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Lines ◽  
Cell Cycle Progression ◽  
Radiation Treatment ◽  
Radiation Sensitivity ◽  
Future Research ◽  
Mtor Inhibition ◽  
Mutational Status ◽  
Intrinsic Radiosensitivity

Abstract Background: Radiotherapy is routinely used to combat glioblastoma multiforme (GBM). However, the treatment efficacy is often limited by the radioresistance of GBM cells.Methods: Two isogenic GBM lines MO59K and MO59J, differing in intrinsic radiosensitivity and mutational status of DNA-PK and ATM, were analyzed regarding their response to DNA-PK/PI3K/mTOR inhibition by PI-103 in combination with radiation. To this end we assessed colony-forming ability, induction and repair of DNA damage by γH2AX, expression of marker proteins, including those belonging to NHEJ and HR repair pathways, degree of apoptosis, autophagy, and cell cycle alterations.Results: We found that PI-103 radiosensitized MO59K cells but, surprisingly, it induced radiation resistance in MO59J cells. In MO59K cells, combined PI-103 and radiation treatment induced much higher γH2AX expression measured by Western blot as compared to MO59J. Another cell line-specific difference includes diminished expression of p53 in MO59J cells, which was further reduced by PI-103. Additionally, PI-103-treated MO59K cells exhibited an increased expression of the apoptosis marker cleaved PARP. In contrast, PI-103-treated MO59J cells showed an increased level of LC3BII, indicative of cytoprotective autophagy. Moreover, irradiation induced a strong G2 arrest in MO59J cells (~80% vs. ~50% in MO59K), which was, however, partially abolished by PI-103 thus allowing cell-cycle progression of a fraction of cells. In contrast, treatment with PI-103 increased the G2 fraction in irradiated MO59K cells.Conclusions: The triple-target inhibitor PI-103 exerted radiosensitization on MO59K cells, but, unexpectedly, caused radioresistance in the MO59J line, lacking DNA-PK. The difference is most likely due to low expression of the DNA-PK substrate p53 in MO59J cells, which was further reduced by PI-103. This led to less apoptosis as compared to drug-free MO59J cells and enhanced survival via partially abolished cell-cycle arrest. The findings suggest that the lack of DNA-PK-dependent NHEJ in MO59J line might be compensated by DNA-PK independent DSB repair via a yet unknown mechanism. Future research on an extended cell panel should focus on finding ways to enhance the radiosensitivity of cell lines with deficiencies in DNA-PK and ATM, the key proteins involved in the DNA damage response.

Overview of Mechanisms of Action of Lycopene

2002 ◽  
Vol 227 (10) ◽  
pp. 920-923 ◽  
Author(s):  
David Heber ◽  
Qing-Yi Lu
Keyword(s):  
Cell Cycle ◽  
Connexin 43 ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Future Research ◽  
Dietary Intakes ◽  
Cycle Progression ◽  
Junctional Communication

Dietary intakes of tomatoes and tomato products containing lycopene have been shown to be associated with decreased risk of chronic diseases such as cancer and cardiovascular diseases in numerous studies. Serum and tissue lycopene levels have also been inversely related to the risk of lung and prostate cancers. Lycopene functions as a very potent antioxidant, and this is clearly a major important mechanism of lycopene action. In this regard, lycopene can trap singlet oxygen and reduce mutagenesis in the Ames test. However, evidence is accumulating for other mechanisms as well. Lycopene at physiological concentrations can inhibit human cancer cell growth by interfering with growth factor receptor signaling and cell cycle progression specifically in prostate cancer cells without evidence of toxic effects or apoptosis of cells. Studies using human and animal cells have identified a gene, connexin 43, whose expression is upregulated by lycopene and which allows direct intercellular gap junctional communication (GJC). GJC is deficient in many human tumors and its restoration or upregulation is associated with decreased proliferation. The combination of low concentrations of lycopene with 1, 25-dihydroxyvitamin D3 exhibits a synergistic effect on cell proliferation and differentiation and an additive effect on cell cycle progression in the HL-60 promyelocyte leukemia cell line, suggesting some interaction at a nuclear or subcellular level. The combination of lycopene and lutein synergistically interact as antioxidants, and this may relate to specific positioning of different carotenoids in membranes. This review will focus on the growing body of evidence that carotenoids have unexpected biologic effects in experimental systems, some of which may contribute to their cancer preventive properties in models of carcinogenesis. Consideration of solubility In vitro, comparison with doses achieved in humans by dietary means, interactions with other phytochemicals, and other potential mechanisms such as stimulation of xenoblotic metabolism, inhibition of cholesterogenesis, modulation of cyclooxygenase pathways, and inhibition of inflammation will be considered. This review will point out areas for future research where more evidence is needed on the effects of lycopene on the etiology of chronic disease.

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