UV‐B‐ and oxidative stress‐induced increase in nicotinamide and trigonelline and inhibition of defensive metabolism induction by poly(ADP‐ribose)polymerase inhibitor in plant tissue

Berglund, Torkel; Kalbin, Georgi; Strid, Åke; Rydström, Jan; Ohlsson, Anna B.

doi:10.1016/0014-5793(96)00027-0

Cited by 58 publications

(49 citation statements)

References 42 publications

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“…PARP inhibitor studies have demonstrated the involvement of PARPs in abiotic stress (Amor et al, 1998;De Block et al, 2005) and defense responses (Berglund et al, 1996;Adams-Phillips et al, 2008). A role for PARP activity in seeds to protect against genotoxic stress has also been inferred (Hunt and Gray, 2009).…”

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confidence: 99%

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

2009

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RADICAL-INDUCED CELL DEATH1 (RCD1) and SIMILAR TO RCD ONE1 (SRO1) are the only two proteins encoded in the Arabidopsis (Arabidopsis thaliana) genome containing both a putative poly(ADP-ribose) polymerase catalytic domain and a WWE protein-protein interaction domain, although similar proteins have been found in other eukaryotes. Poly(ADP-ribose) polymerases mediate the attachment of ADP-ribose units from donor NAD + molecules to target proteins and have been implicated in a number of processes, including DNA repair, apoptosis, transcription, and chromatin remodeling. We have isolated mutants in both RCD1 and SRO1, rcd1-3 and sro1-1, respectively. rcd1-3 plants display phenotypic defects as reported for previously isolated alleles, most notably reduced stature. In addition, rcd1-3 mutants display a number of additional developmental defects in root architecture and maintenance of reproductive development. While single mutant sro1-1 plants are relatively normal, loss of a single dose of SRO1 in the rcd1-3 background increases the severity of several developmental defects, implying that these genes do share some functions. However, rcd1-3 and sro1-1 mutants behave differently in several developmental events and abiotic stress responses, suggesting that they also have distinct functions. Remarkably, rcd1-3; sro1-1 double mutants display severe defects in embryogenesis and postembryonic development. This study shows that RCD1 and SRO1 are at least partially redundant and that they are essential genes for plant development.

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The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

2009

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“…Determination of nicotinamide and trigonelline coneentrations. The plant material ("1 g) was weighed, triturated with sand, extracted and quantified according to Berglund et al (1996). To be able to directly compare the different results in this report, be it from nicotinamide, trigonelline, GSH or transcript level determinations, and to avoid diurnal variations, the results were all expressed as percentage of the initial control sample of each measurement.…”

Section: Methodsmentioning

confidence: 99%

“…The present study was conducted in order to further elucidate the effect of UV-B radiation, low and high doses, on the accumulation of nicotinamide and trigonelline in plant tissue, which was shown in Berglund et al (1996) and on the level of oxidative processes (manifested as changes in GSWGSSG) and mRNA levels of defence-related and other proteins. Especially we wanted to investigate any relationship between UV-B-induced changes in nicotinamide or trigonelline levels and the expression of defence genes in connection with oxidative stress.…”

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confidence: 99%

Ultraviolet‐B‐Radiation‐Induced Changes in Nicotinamide and Glutathione Metabolism and Gene Expression in Plants

Kalbin

Ohlsson

Berglund

et al. 1997

European Journal of Biochemistry

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Pea (Pisum sativum L. cv. Greenfeast) plants were exposed to supplementary ultraviolet‐B (UV‐B) radiation (biologically effective dose rates normalised to 300 nm, UV‐BBE300: 0.18, 0.32 or 1.4 W m−2). Leaf nicotinamide, trigonelline, GSHtot (total glutathione) and GSSG (oxidised glutathione) levels remained unchanged after exposure to the lowest dose rates. 1.4 W m−2 UV‐BBE,300: gave rise to 60‐fold and 4.5‐fold increases in GSSG and GSHtot, respectively. 3.5‐fold and 9.5‐fold increases were found in nicotinamide and trigonelline, respectively, cab (Chlorophyll‐a/b‐binding protein) transcript levels decreased and CHS (chalcone synthase) and PAL (phenylalanine ammonia‐lyase) mRNA increased after shorter UV‐B exposures (hours) to the higher dose rate of UV‐B, and after exposure to the intermediate dose rate. CHS and PAL mRNAs also increased after prolonged exposure to the lowest dose rate. cah transcripts completely disappeared, whereas CHS and PAL mRNA levels rose by 60‐fold and 17‐fold, respectively, after 12 h exposure at the highest dose rate and 12 h of development. Our results indicate that nicotinamide or trigonelline do not function as signalling compounds for CHS and PAL gene expression. Elevated nicotinamide and trigonelline levels occur in response to UV‐B, but only at UV‐B doses high enough to cause oxidative stress.

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“…Despite the old5 mutation, pyridine nucleotide levels in the mutant were increased compared with the wild type. This might be due to the activation of a stress response program, since increased expression of the NAD salvage pathway is reminiscent of the need to replenish the NAD pool during stress conditions (Berglund et al, 1996;Hunt et al, 2007;Wang and Pichersky, 2007). One example of a NAD-consuming enzyme induced by oxidative stress is poly(ADP-ribose) polymerase (De Block et al, 2005), linking increased salvage metabolism to stress.…”

Section: Pyridine Biosynthesis Crosstalk and Stress Programming In mentioning

confidence: 99%

TheArabidopsis onset of leaf death5Mutation of Quinolinate Synthase Affects Nicotinamide Adenine Dinucleotide Biosynthesis and Causes Early Ageing

et al. 2008

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Leaf senescence in Arabidopsis thaliana is a strict, genetically controlled nutrient recovery program, which typically progresses in an age-dependent manner. Leaves of the Arabidopsis onset of leaf death5 (old5) mutant exhibit early developmental senescence. Here, we show that OLD5 encodes quinolinate synthase (QS), a key enzyme in the de novo synthesis of NAD. The Arabidopsis QS was previously shown to carry a Cys desulfurase domain that stimulates reconstitution of the oxygen-sensitive Fe-S cluster that is required for QS activity. The old5 lesion in this enzyme does not affect QS activity but it decreases its Cys desulfurase activity and thereby the long-term catalytic competence of the enzyme. The old5 mutation causes increased NAD steady state levels that coincide with increased activity of enzymes in the NAD salvage pathway. NAD plays a key role in cellular redox reactions, including those of the tricarboxylic acid cycle. Broad-range metabolite profiling of the old5 mutant revealed that it contains higher levels of tricarboxylic acid cycle intermediates and nitrogen-containing amino acids. The mutant displays a higher respiration rate concomitant with increased expression of oxidative stress markers. We postulate that the alteration in the oxidative state is integrated into the plant developmental program, causing early ageing of the mutant.

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UV‐B‐ and oxidative stress‐induced increase in nicotinamide and trigonelline and inhibition of defensive metabolism induction by poly(ADP‐ribose)polymerase inhibitor in plant tissue

Abstract: Nicotinamide and trigoneUine contents increased in

Cited by 58 publications

References 42 publications

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

Ultraviolet‐B‐Radiation‐Induced Changes in Nicotinamide and Glutathione Metabolism and Gene Expression in Plants

TheArabidopsis onset of leaf death5Mutation of Quinolinate Synthase Affects Nicotinamide Adenine Dinucleotide Biosynthesis and Causes Early Ageing

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