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Synonyms
chlorophyll b reductase, non-yellow coloring 1, chl b reductase, non-yellow coloring1, nyc1-like, chlorophyll(ide) b reductase, bonyc1, lpnyc1,
more
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71-hydroxychlorophyllide a + NADP+
chlorophyllide b + NADPH + H+
chlorophyll b + NADPH
7-hydroxymethyl chlorophyll a + NADP+
chlorophyll b + NADPH
? + NADP+
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?
chlorophyllide b + NAD(P)H + H+
71-hydroxychlorophyllide a + NAD(P)+
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r
chlorophyllide b + NADPH + H+
7-hydroxychlorophyllide a + NADP+
zinc (132R)-pheophorbide b + NADPH + H+
?
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zinc (132S)-pheophorbide b is a better substrate than zinc (132R)-pheophorbide b
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?
zinc (132S)-pheophorbide b + NADPH + H+
?
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zinc (132S)-pheophorbide b is a better substrate than zinc (132R)-pheophorbide b
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?
Zn-pheophorbide b + NADPH + H+
?
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?
additional information
?
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chlorophyll b reduction is considered to be an early and obligatory step of chlorophyll b breakdown
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?
71-hydroxychlorophyllide a + NADP+

chlorophyllide b + NADPH + H+
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?
71-hydroxychlorophyllide a + NADP+
chlorophyllide b + NADPH + H+
chlorophyll b is important for LHCP stability, and no pigment-bound LHCP is detected in chlorophyll b-deficient mutants
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?
71-hydroxychlorophyllide a + NADP+
chlorophyllide b + NADPH + H+
the enzyme NYC1 is required for proper chloroplast degeneration, chlorophyll b is important for LHCP stability, and no pigment-bound LHCP is detected in chlorophyll b-deficient mutants
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?
chlorophyll b + NADPH

7-hydroxymethyl chlorophyll a + NADP+
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?
chlorophyll b + NADPH
7-hydroxymethyl chlorophyll a + NADP+
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when purified trimeric photosystem II is incubated with recombinant chlorophyll b reductase (NOL), conversion of chlorophyll b in photosystem II to 7-hydroxymethyl chlorophyll a. Chlorophyll b reductase catalyzes the initial step of photosystem II degradation
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?
chlorophyll b + NADPH
7-hydroxymethyl chlorophyll a + NADP+
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catalyzed by recombinant NOL, whereas NYC1 protein alone shows no activity, but it is required for a functional chlorophyll b reductase
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?
chlorophyllide b + NADPH + H+

7-hydroxychlorophyllide a + NADP+
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-
-
-
?
chlorophyllide b + NADPH + H+
7-hydroxychlorophyllide a + NADP+
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-
-
-
?
chlorophyllide b + NADPH + H+
7-hydroxychlorophyllide a + NADP+
-
-
-
-
?
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71-hydroxychlorophyllide a + NADP+
chlorophyllide b + NADPH + H+
chlorophyllide b + NAD(P)H + H+
71-hydroxychlorophyllide a + NAD(P)+
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-
-
r
chlorophyllide b + NADPH + H+
7-hydroxychlorophyllide a + NADP+
additional information
?
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chlorophyll b reduction is considered to be an early and obligatory step of chlorophyll b breakdown
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-
?
71-hydroxychlorophyllide a + NADP+

chlorophyllide b + NADPH + H+
chlorophyll b is important for LHCP stability, and no pigment-bound LHCP is detected in chlorophyll b-deficient mutants
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-
?
71-hydroxychlorophyllide a + NADP+
chlorophyllide b + NADPH + H+
the enzyme NYC1 is required for proper chloroplast degeneration, chlorophyll b is important for LHCP stability, and no pigment-bound LHCP is detected in chlorophyll b-deficient mutants
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?
chlorophyllide b + NADPH + H+

7-hydroxychlorophyllide a + NADP+
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?
chlorophyllide b + NADPH + H+
7-hydroxychlorophyllide a + NADP+
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-
-
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?
chlorophyllide b + NADPH + H+
7-hydroxychlorophyllide a + NADP+
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-
-
-
?
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brenda
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expression of NYC1 during embryo development and regulation, semiquantitative reverse transcription-PCR analysis, overview
brenda
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brenda
low expression level
brenda
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innercellular structures of the enzyme wild-type and mutant seeds
brenda
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brenda
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of wild-type
brenda
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during fruit development, no obvious change of chlorophyll b reductase mRNA is found. Chlorophyll loss is greatly accelerated by postharvest ethylene fumigation, and NYC transcript abundance is only related to accelerated chlorophyll degradation in ethylene-induced degreening
brenda
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during fruit development, no obvious change of chlorophyll b reductase mRNA is found. Chlorophyll loss is greatly accelerated by postharvest ethylene fumigation, and NYC transcript abundance is only related to accelerated chlorophyll degradation in ethylene-induced degreening
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brenda
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chlorophyll b is associated with LHC proteins
brenda
low abundance of mRNA and protein in green leaves, levels increase in response to dark-induced senescence
brenda
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of a light-grown chlorophyll-deficient mutant of Helianthus annuus
brenda
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a pronounced maximum of Chl b reductase activity at day 2 of senescence
brenda
expression in leaf sheaths is detectable but is significantly lower than those in expanding and mature leaves. During the progression of natural leaf senescence at 24, 30, and 36 d after leaf emergence, the expression levels of LpNYC1 increase and are approximately 23.1, 38.8, and 148.7times higher than those at the expanding stage (12 d after leaf emergence), respectively
brenda
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brenda
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brenda
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brenda
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brenda
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brenda
low expression level
brenda
additional information

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isozymes NOL and NYC1 are differentially expressed in Arabidopsis during development
brenda
additional information
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BoNYC1 expression increases during first days of postharvest, but decreases in advanced senescence stages, simultaneously with chlorophyll degradation. Treatments with cytokinins and 1-MCP delays the increment of BoNYC1 expression whereas ethylene accelerates the process
brenda
additional information
the expression pattern is correlated with the progression of leaf senescence
brenda
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additional information
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rice mutants lacking either NYC1 or NOL are deficient in chlorophyll b reductase activity during leaf senescence. Recombinant NOL enzyme shows in vitro chlorophyll b reductase activity in the absence of NYC1, it is possible that NOL could function independently of NYC1. It is possible that the heterodimer formation of NYC1 and NOL is necessary only under specific developmental conditions such as leaf senescence
evolution

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chlorophyll b reductase belongs to the short-chain dehydrogenase superfamily
evolution
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chlorophyll b reductase belongs to the short-chain dehydrogenase superfamily
evolution
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chlorophyll b reductase belongs to the short-chain dehydrogenase superfamily
evolution
LpNYC1 shares the highest amino acid sequence similarity with BdNYC1 (91.5%) in Brachypodium distachyon, and the lowest with Arabidopsis NYC1 (63.6%). Despite the sequence divergence, the NYC1 orthologues all share the classical chloroplast-localized short-chain dehydrogenase/reductase (SDR) domain with the TGXXGXXG cofactor binding motif and the YXXXK active site for catabolizing Chl b into 7-hydroxymethyl-chl a
malfunction

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Arabidosis thaliana mutants lacking either NYC1 or NOL are deficient in chlorophyll b reductase activity during leaf senescence. Impairment in the chlorophyll b reduction leads to LHC stabilization during leaf senescence in the rice mutant lacking chlorophyll b reductase
malfunction
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germination rates of mutants rapidly decrease during storage, the non-yellow coloring1 (nyc1)/nyc1-like (nol) mutant seeds fail to germinate after storage for 23 months, whereas 75% of the wild-type seeds germinate after 42 months. Mutations in the chlorophyll degradation enzymes, e.g. in chlorophyll b reductase, result in the stay-green phenotype in leaves, only a nyc1 mutation was accompanied by a stay-green phenotype in Arabidopsis thaliana. Lack of chlorophyll b reductase results in the retention of LHC proteins as well as both chlorophyll a and b that are associated with LHC proteins in leaves. Large amount of LHCII apoproteins accumulated in the nyc1 and nyc1/nol mutants
malfunction
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rice mutants lacking either NYC1 or NOL are deficient in chlorophyll b reductase activity during leaf senescence. Impairment in the chlorophyll b reduction leads to LHC stabilization during leaf senescence in the rice mutant lacking chlorophyll b reductase
malfunction
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in broccoli, treatments with UV-C can delay Chl degradation, diminish respiration rates and reduce the loss of sugars and proteins during postharvest storage
malfunction
knocking out the Chl b reductase gene might lead to a stay-green phenotype. Overexpression of LpNYC1 activates leaf senescence in Nicotiana benthamiana and rescues the stay-green trait in the Arabidopsis thaliana nyc1 null mutant
metabolism

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the enzyme is part of the chlorophyll metabolism pathway, overview. Chlorophyll b reductase catalyzes the conversion of chlorophyll b to 7-hydroxymethyl chlorophyll a, which is the first step in chlorophyll b degradation
metabolism
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three enzymes participating in the chlorophyll cycle, namely, chlorophyllide a oxygenase, chlorophyll b reductase, and 7-hydroxymethylchlorophyll reductase, overview. In the reverse reactions from chlorophyll b to chlorophyll a, the 7-formyl group of chlorophyll b is first reduced to a hydroxyl group by the action of chlorophyll b reductase. The activities of chlorophyll b reductase and7-hydroxymethylchlorophyll reductase are coordinated in their regulation, otherwise, imbalance of those activities may lead to accumulation of the intermediate of the pathway. The conversion of chlorophyll b into chlorophyll a precedes the degradation of LHC during leaf senescence
metabolism
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three enzymes participating in the chlorophyll cycle, namely, chlorophyllide a oxygenase, chlorophyll b reductase, and 7-hydroxymethylchlorophyll reductase, overview. In the reverse reactions from chlorophyll b to chlorophyll a, the 7-formyl group of chlorophyll b is first reduced to a hydroxyl group by the action of chlorophyll b reductase. The activities of chlorophyll b reductase and7-hydroxymethylchlorophyll reductase are coordinated in their regulation, otherwise, imbalance of those activities may lead to accumulation of the intermediate of the pathway. The conversion of chlorophyll b into chlorophyll a precedes the degradation of LHC during leaf senescence
metabolism
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three enzymes participating in the chlorophyll cycle, namely, chlorophyllide a oxygenase, chlorophyll b reductase, and 7-hydroxymethylchlorophyll reductase, overview. In the reverse reactions from chlorophyll b to chlorophyll a, the 7-formyl group of chlorophyll b is first reduced to a hydroxyl group by the action of chlorophyll b reductase. The activities of chlorophyll b reductase and7-hydroxymethylchlorophyll reductase are coordinated in their regulation, otherwise, imbalance of those activities may lead to accumulation of the intermediate of the pathway. The conversion of chlorophyll b into chlorophyll a precedes the degradation of LHC during leaf senescence
metabolism
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during senescence, chlorophylls are degraded with the purpose of avoiding presence of photoactive molecules. Chlorophyll b must be previously converted to chlorophyll a in order to be catabolized. This reduction process is catalyzed by two enzymes, chlorophyll b reductase (CBR) and hydroxymethyl chlorophyll a reductase (HCAR)
physiological function

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chlorophyll b reductase plays an essential role in maturation and storability of seeds. Both isozymes NYC1 and NOL participate in chlorophyll degradation during seed maturation
physiological function
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when greening seedlings are transferred back to darkness, conversion of chlorophyll b to chlorophyll a occurs, which results in degradation of LHC and an increase in the core antenna complexes
physiological function
inflorescence degreening is associated with increased mRNA abundance of NYC1, pheophytin pheophorbide hydrolase and pheophorbide a oxygenase. Mutants of NYC1 show preferential retention of chlorophyll b during dark incubation
physiological function
isoform NYC1 degrades the chlorophyll b on photosystem II under high-light conditions, thus decreasing the photosystem II content. During high-light treatment, the chlorophyll a/b ratio is stable in the wild-type and plants lacking NYC1-Like (NOL) activity, and the photosystem II content decreases in wiild-type plants. The chlorophyll a/b ratio decreases in the NYC1 and NYC1/NOL deficient plants, and a substantial degree of photosystem II is retained in NYC1/NOL deficient plants after the high-light treatment
physiological function
NOL is not the primary enzyme responsible for degradation. During high-light treatment, the chlorophyll a/b ratio is stable in the wild-type and plants lacking NYC1-Like (NOL) activity, and the photosystem II content decreases in wiild-type plants. The chlorophyll a/b ratio decreases in NYC1/NOL deficient plants, and a substantial degree of photosystem II is retained in NYC1/NOL deficient plants after the high-light treatment
physiological function
when the level of chlorophyll b is enhanced by the introduction of a truncated chlorophyllide a oxygenase gene and leaves are incubated in the dark, the amount of NYC1 is greatly increased compared while the amount of NYC1 mRNA is the same as in the wild type. In contrast, NYC1 does not accumulate in the mutant without chlorophyll b. The NYC1 level is related to the energetically uncoupled light-harvesting chlorophyll a/b protein complex
physiological function
chlorophyll (Chl) degradation leads to leaf senescence and adversely affects biomass production of forage grasses and aesthetic appearance of turfgrasses. Transcriptional regulation of chlorophyll b reductase gene non-yellow coloring 1 associated with leaf senescence in perennial ryegrass. Predicted functional roles of LpNYC1 in Chl catabolism in green tissues and in leaf senescence. LpNYC1 catalyzes Chl degradation. Upstream transcription factors from Lolium perenne, LpABI5, LpABF3, and LpEIN3, directly regulating the expression of LpNYC1 in perennial ryegrass during leaf senescence
physiological function
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chlorophyll molecules (Chl a and Chl b) are located in the thylakoid membranes inside the chloroplasts forming part of the light-harvesting chlorophyll a/b-protein complex of photosystem II (LHCII). During senescence, thylakoid membranes are dismantled and chlorophyll molecules are released and catabolized. Chlorophyll degradation is under strict control because free chlorophyll molecules or their intermediates are photoactive and can generate highly reactive toxic radicals. During senescence, chlorophylls are degraded, therefore chlorophyll b must be previously converted to chlorophyll a in order to be catabolized. This reduction process is catalyzed by two enzymes, chlorophyll b reductase (CBR) and hydroxymethyl chlorophyll a reductase (HCAR). Chlorophyll b degradation is required for the degradation of light-harvesting complex II and thylakoid grana during leaf senescence
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NOL_ARATH
348
0
38149
Swiss-Prot
Chloroplast (Reliability: 3)
NOL_ORYSJ
343
0
37004
Swiss-Prot
Chloroplast (Reliability: 5)
NYC1_ARATH
496
3
54845
Swiss-Prot
other Location (Reliability: 5)
NYC1_ORYSJ
504
3
54716
Swiss-Prot
Mitochondrion (Reliability: 5)
A0A2I0BG17_9ASPA
240
0
25513
TrEMBL
Mitochondrion (Reliability: 5)
A0A7C8YQ47_OPUST
265
0
29338
TrEMBL
Chloroplast (Reliability: 1)
A0A7C8YQS1_OPUST
100
0
11070
TrEMBL
other Location (Reliability: 2)
A0A2H1IET3_9MICO
258
0
27185
TrEMBL
-
A0A7C9CS00_OPUST
107
0
11566
TrEMBL
other Location (Reliability: 2)
A0A2G9HNM6_9LAMI
157
0
17430
TrEMBL
other Location (Reliability: 5)
A0A7C8YQ64_OPUST
206
0
23315
TrEMBL
other Location (Reliability: 3)
A0A7C8YQA0_OPUST
329
0
35731
TrEMBL
Chloroplast (Reliability: 1)
A0A7C8YQ46_OPUST
319
0
34609
TrEMBL
Chloroplast (Reliability: 1)
A0A0D2LJR1_9CHLO
138
0
14937
TrEMBL
other Location (Reliability: 3)
A0A2I0AW38_9ASPA
71
0
7891
TrEMBL
other Location (Reliability: 4)
A0A2I0B946_9ASPA
521
3
56376
TrEMBL
Chloroplast (Reliability: 3)
A0A0B2SKU7_GLYSO
515
3
56596
TrEMBL
other Location (Reliability: 5)
G7KPV9_MEDTR
514
3
56489
TrEMBL
other Location (Reliability: 4)
G7KPV9_MEDTR
514
3
56489
TrEMBL
other Location (Reliability: 4)
A0A2P6RJG3_ROSCH
501
3
54306
TrEMBL
Chloroplast (Reliability: 5)
A0A7C9EJR3_OPUST
514
3
56541
TrEMBL
Chloroplast (Reliability: 5)
A0A1Z5K9Q9_FISSO
329
0
35409
TrEMBL
Secretory Pathway (Reliability: 4)
A0A072TQT8_MEDTR
341
0
37630
TrEMBL
Chloroplast (Reliability: 1)
A0A2P6SBL7_ROSCH
340
0
37809
TrEMBL
Chloroplast (Reliability: 2)
A0A1Z5KAT7_FISSO
328
0
35313
TrEMBL
Secretory Pathway (Reliability: 2)
A0A7C9CUK0_OPUST
100
0
11165
TrEMBL
other Location (Reliability: 5)
A0A0B2SPT9_GLYSO
237
0
26822
TrEMBL
Mitochondrion (Reliability: 3)
A0A7C9CY41_OPUST
208
0
23545
TrEMBL
other Location (Reliability: 2)
A0A0B2QX29_GLYSO
349
0
38258
TrEMBL
Chloroplast (Reliability: 1)
A0A0D2J150_9CHLO
138
0
14764
TrEMBL
other Location (Reliability: 5)
A0A2G9HPN2_9LAMI
523
2
57298
TrEMBL
other Location (Reliability: 5)
A0A2I0AJW8_9ASPA
213
0
23718
TrEMBL
other Location (Reliability: 4)
A0A2I0AW51_9ASPA
71
0
8270
TrEMBL
other Location (Reliability: 4)
A0A7C8YQS4_OPUST
207
0
23461
TrEMBL
other Location (Reliability: 2)
A0A2G9GAE1_9LAMI
173
0
19107
TrEMBL
other Location (Reliability: 2)
A0A0D2K662_9CHLO
445
0
46146
TrEMBL
Secretory Pathway (Reliability: 5)
A0A1Q1NIA8_LOLPR
495
0
53502
TrEMBL
-
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P360S
mutation changes the 3D structure of the NADPH binding site, leading to delays in postharvest degreening
additional information

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a double mutant constructed between nyc1 and cao (enzyme for chlorophyll b biosynthesis) fails to display a stay-green phenotype during dark-induced senescence
additional information
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Arabidopsis nol/nyc1 double mutant, when the genes for chlorophyll b reductases NOL and NYC1 are disrupted, chlorophyll b and photosystem II are not degraded during senescence, whereas other pigment complexes completely disappear
additional information
a mutation producing a termination codon, and a mutation interfering with correct intron splicing both lead to delays in postharvest degreening
additional information
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analysis of expression of a gene encoding a putative CBR (BoNYC1) during postharvest senescence of broccoli and of effects of postharvest physical treatements, overview
additional information
the non-yellow coloring, nyc1, recessive mutant is a rice stay-green phenotype mutant due to a defect in chlorophyl degradation, in which chlorophyll degradation during senescence is impaired, the mutant NYC1 does not show chlorophyll b reductase activity, but NOL, i.e. NYC1-like, a protein closely related to NYC1 in rice, shows chlorophyll b reductase activity in vitro, phenotype, overview, a double mutant from a cross between nyc1-2 and a chlorophyll b-deficient mutant cao-2 does not show the stay-green senescence phenotype, overview
additional information
the non-yellow coloring, nyc1, recessive mutant is a rice stay-green phenotype mutant due to a defect in chlorophyl degradation, in which chlorophyll degradation during senescence is impaired, the mutant NYC1 does not show chlorophyll b reductase activity, but NOL, i.e. NYC1-like, a protein closely related to NYC1 in rice, shows chlorophyll b reductase activity in vitro, phenotype, overview, a double mutant from a cross between nyc1-2 and a chlorophyll b-deficient mutant cao-2 does not show the stay-green senescence phenotype, overview
additional information
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the non-yellow coloring, nyc1, recessive mutant is a rice stay-green phenotype mutant due to a defect in chlorophyl degradation, in which chlorophyll degradation during senescence is impaired, the mutant NYC1 does not show chlorophyll b reductase activity, but NOL, i.e. NYC1-like, a protein closely related to NYC1 in rice, shows chlorophyll b reductase activity in vitro, phenotype, overview, a double mutant from a cross between nyc1-2 and a chlorophyll b-deficient mutant cao-2 does not show the stay-green senescence phenotype, overview
additional information
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nyc1 mutant, shows the stay-green phenotype. Nol mutant (lines G079-11B, C130-10H and G087-9H) shows a stay-green phenotype very similar to that of the nyc1 mutant, i.e. the degradation of chlorophyll b is severely inhibited and light-harvesting complex II is selectively retained during senescence, resulting in the retention of thylakoid grana even at a late stage of senescence. The nyc1 nol double mutant does not show prominent enhancement of inhibition of chlorophyll degradation
additional information
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nyc1-mutant is a stay-green mutant. The double mutant nyc1/nol only slightly enhances the corresponding single mutant phenotypes
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coding region of chlorophyll b reductase (NOL) lacking its transit peptide amplified and cloned into pET-30a(+) at NspV and HindIII sites, expressed in Escherichia coli Rosetta DE3
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fusion of the region encoding the putative transit peptide of NOL to the green fluorescent protein (GFP) gene and introduced into the epidermal cells of Allium cepa by particle bombardment
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gene nol, DNA and amino acid determination and anaylsis, phylogenetic tree, promoter analysis, semiquantitative RT-PCR expression analysis, overview
gene NYC1, cloned using the RACE-PCR method, DNA and amino acid sequence determination and analysis, sequence comparisons and phylogenetic analysis, semiquantitative and quantitative RT-PCR enzyme expression analysis, transient overexpression of LpNYC1 in wild-type Nicotiana benthamiana under control of CaMV 35S promoter and in Arabidopsis thaliana nyc1 null mutant strain AGL1, both via Agrobacterium tumefaciens transfection, recombinant expression of GFP-tagged enzyme NYC1 in Lolium perenne protoplasts
gene nyc1, DNA and amino acid determination and anaylsis, phylogenetic tree, promoter analysis, semiquantitative RT-PCR expression analysis, overview
gene NYC1, real-time PCR enzyme expression analysis
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genes nyc1 and nol, the NYC1 promoter contains a potential abscisic acid-responsive element, semiquantitative reverse transcription-PCR expression analysis of isozymes
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positional cloning of nyc1
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Chlorophyll loss in fruit peel is greatly accelerated by postharvest ethylene fumigation, which greatly increases the expression of chlorophyll b reductase NYC and chlorophyllase Chlase. The increase in Chlase and NYC transcript abundance is only related to accelerated chlorophyll degradation in ethylene-induced degreening
cytokinins and 1-MCP inhibit developmental increase in BoNYC1 expression. Samples treated with heat show a significant lower relative expression of BoNYC1 in comparison to controls after 72 h but not after 120 h of storage
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ethylene, via 2-chloroethylphosphonic acid (ethephon, an ethylene-releasing agent), enhances developmental increase in BoNYC1 expression. Samples treated with visible light show a higher increment of BoNYC1 expression in relation to controls after 72 h but the expression is similar to those of controls after 120 h. Expressions of NYC1 and its homologue, NOL, increase markedly under intense light conditions
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expression of LpNYC1 is highly inducible by abscisic acid (ABA) and ethephon (ethylene releasing reagent). Transcription factors LpABI5, LpABF3, and LpEIN3 directly activate the expression of LpNYC1 by binding to its promoter
expression of LpNYC1 is suppressed by treatment with AVG (ethylene biosynthesis inhibitor)
NYC1 expression is repressed in the abscisic acid-insensitive mutants during embryogenesis
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Chlorophyll loss in fruit peel is greatly accelerated by postharvest ethylene fumigation, which greatly increases the expression of chlorophyll b reductase NYC and chlorophyllase Chlase. The increase in Chlase and NYC transcript abundance is only related to accelerated chlorophyll degradation in ethylene-induced degreening

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Chlorophyll loss in fruit peel is greatly accelerated by postharvest ethylene fumigation, which greatly increases the expression of chlorophyll b reductase NYC and chlorophyllase Chlase. The increase in Chlase and NYC transcript abundance is only related to accelerated chlorophyll degradation in ethylene-induced degreening
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