Characterization of natural leaf senescence in tobacco (Nicotiana tabacum) plants grown in vitro

PROTOPLASMA ◽  
2015 ◽  
Vol 253 (2) ◽  
pp. 259-275 ◽  
Author(s):  
Branka Uzelac ◽  
Dušica Janošević ◽  
Ana Simonović ◽  
Václav Motyka ◽  
Petre I. Dobrev ◽  
...  
Planta ◽  
2000 ◽  
Vol 211 (4) ◽  
pp. 510-518 ◽  
Author(s):  
Céline Masclaux ◽  
Marie-Hélène Valadier ◽  
Norbert Brugière ◽  
Jean-François Morot-Gaudry ◽  
Bertrand Hirel

2021 ◽  
Vol 12 ◽  
Author(s):  
Zheng Chen ◽  
Wei Jia ◽  
Songwei Li ◽  
Jiayang Xu ◽  
Zicheng Xu

Melatonin (MEL) is a pleiotropic agent with crucial functions reported in a variety of stress responses and developmental processes. Although MEL involvement in plant defense against natural leaf senescence has been widely reported, the precise regulatory mechanisms by which it delays stress-induced senescence remain unclear. In this study, we found that foliar spraying of melatonin markedly ameliorated dehydration-induced leaf senescence in Nicotiana tabacum, accompanied by attenuated oxidative damage, expression of senescence-related genes, and reduced endogenous ABA production. Metabolite profiling indicated that melatonin-treated plants accumulated higher concentrations of sugars, sugar alcohol, and organic acids, but fewer concentrations of amino acids in the leaves, than untreated plants after exposure to dehydration. Gene expression analysis revealed that the delayed senescence of stressed plants achieved by melatonin treatment might be partially ascribed to the upregulated expression of genes involved in ROS scavenging, chlorophyll biosynthesis, photosynthesis, and carbon/nitrogen balances, and downregulated expression of senescence-associated genes. Furthermore, hormone responses showed an extensively modulated expression, complemented by carotenoid biosynthesis regulation to achieve growth acceleration in melatonin-treated plants upon exposure to dehydration stress. These findings may provide more comprehensive insights into the role of melatonin in alleviating leaf senescence and enhancing dehydration resistance.


1991 ◽  
Vol 66 (04) ◽  
pp. 453-458 ◽  
Author(s):  
John T Brandt

SummaryLupus anticoagulants (LAs) are antibodies which interfere with phospholipid-dependent procoagulant reactions. Their clinical importance is due to their apparent association with an increased risk of thrombo-embolic disease. To date there have been few assays for quantifying the specific activity of these antibodies in vitro and this has hampered attempts to purify and characterize these antibodies. Methods for determining phospholipid-dependent generation of thrombin and factor Xa are described. Isolated IgG fractions from 7 of 9 patients with LAs were found to reproducibly inhibit enzyme generation in these assay systems, permitting quantitative expression of inhibitor activity. Different patterns of inhibitory activity, based on the relative inhibition of thrombin and factor Xa generation, were found, further substantiating the known heterogeneity of these antibodies. These systems may prove helpful in further purification and characterization of LAs.


1992 ◽  
Vol 67 (01) ◽  
pp. 063-065 ◽  
Author(s):  
Sherryl A M Taylor ◽  
Jacalyn Duffin ◽  
Cherie Cameron ◽  
Jerome Teitel ◽  
Bernadette Garvey ◽  
...  

SummaryChristmas disease was first reported as a distinct clinical entity in two manuscripts published in 1952 (1, 2). The eponym associated with this disorder, is the surname of the first patient examined in detail and reported by Biggs and colleagues in a paper describing the clinical and laboratory features of seven affected individuals (3). This patient has severe factor IX coagulant deficiency (less than 0.01 units/ml) and no detectable circulating factor IX antigen (less than 0.01 units/ml). Coding sequence and splice junctions of the factor IX gene from this patient have been amplified in vitro through the polymerase chain reaction (PCR). One nucleotide substitution was identified at nucleotide 30,070 where a guanine was replaced by a cytosine. This mutation alters the amino acid encoded at position 206 in the factor IX protein from cysteine to serine. The non conservative nature of this substitution, the absence of this change in more than 200 previously sequenced factor IX genes and the fact that the remainder of the coding region of this gene was normal, all provide strong circumstantial evidence in favour of this change being the causative mutation in this patient. The molecular characterization of this novel mutation in the index case of Christmas disease, contributes to the rapidly expanding body of knowledge pertaining to Christmas disease pathogenesis.


Author(s):  
Markus Boel ◽  
Oscar J. Abilez ◽  
Ahmed N Assar ◽  
Christopher K. Zarins ◽  
Ellen Kuhl

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