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Water Deficit in Pea Root Tips: Effects on the Cell Cycle and on the Production of Dehydrin-like Proteins 总被引:3,自引:0,他引:3
BRACALE MARCELLA; LEVI MARISA; SAVINI CHRISTIAN; DICORATO WALTER; GALLI MARIA GRAZIA 《Annals of botany》1997,79(6):593-600
Dehydrin-like proteins have been detected in nuclei and cytoplasmof meristematic root tip cells from pea seedlings subjectedto slow dehydration at 90% relative humidity for 48 h or more.Evidence was gained from Western blotting and immunocytochemicalexperiments using an antibody raised against the conserved domainof dehydrin proteins. Flow cytometer analysis has shown thatcycling cells of root tip meristems from dehydrated seedlingsare mostly arrested in G2 phase. Other stress treatments thoughtto involve water depletion (osmotic stress, cold treatment)or to modulate cell response to water deficit (abscisic acid)gave less clear-cut results with all treatments lowering theproportion of cells entering the S phase, but without a definiteand persistent arrest in any preferential phase of the cycle.Possible interrelationships between G2 arrest and dehydrin productionare discussed. Cell cycle; dehydrins; flow cytometry; nuclei; pea; Pisum sativum L.; water stress 相似文献
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MILENA MARSONI CARLO CANTARA MARIA CONCETTA DE PINTO COSIMO GADALETA LAURA DE GARA MARCELLA BRACALE CANDIDA VANNINI 《Plant, cell & environment》2010,33(7):1161-1175
Tobacco (Nicotiana tabacum) Bright Yellow‐2 (TBY‐2) cells undergo different fates when exposed for 10 minutes to heat stresses of different severity. A 35 °C treatment causes a homeostatic response (HRE) allowing cells to cope with the stress; 55 °C triggers processes leading to programmed cell death (PCD), which is complete after 72 h. We have used a proteomic approach to gain insight into the molecular mechanisms defining the fate of TBY‐2 cells induced by these two heat stresses. Tandem mass spectrometry (MS/MS) and two‐dimensional electrophoresis (2‐DE) analysis revealed little overlap of differentially‐accumulated proteins: the different severities of heat treatment induced the modulation of specific proteins, some of which are responsible for different cell fates. When the imposed heat shock is beyond a certain threshold, the overall reduced metabolism may be the result of a series of events involving gene expression and oxidative damage that would lead to PCD. Our data suggest that the down‐accumulation of several proteins involved in cellular redox homeostasis could provide, until now, an unappreciated contribution to understanding how many partners are involved in promoting the redox impairment leading to PCD. Moreover post‐translational modifications seem to play important regulatory roles in the adaptation of TBY‐2 cells to different intensities of heat stress. 相似文献
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