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Fig 1.

The positions of mutations and expression of DRD1 gene.

(A) Domain structures of DRD1 and DDM1 and positions of drd1-6, drd1-p and ddm1-2. Amino acid sequence change from tryptophan (W) to stop codon in helicase superfamily C-terminal (HELICc) domain in drd1-6. The triangle indicates the position of T-DNA insertion in drd1-p mutant. In case of ddm1-2, substitution of G to A in the splice donor site of intron 11 brings about lack of helicase superfamily C-terminal (HELICc) domain. (B) RT-PCR analysis of DRD1 and control ACTIN2 genes in WT and drd1-p mutant leaves. The drd1-p mutant displayed a decrease in DRD1 expression levels compared to WT.

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Fig 1 Expand

Fig 2.

Delayed leaf senescence symptoms in the drd1-6 mutant.

(A) Phenotypes of 28-day-old and 55-day-old wild-type (WT) and drd1-6 mutant whole plants. (B) Individually darkened leaf (IDL) senescence of WT (left) and drd1-6 (right) plants. Rosette leaves of 28-day-old WT and drd1-6 mutant (IDL 0 d) were induced to undergo senescence for 5 d under dark conditions (IDL 5 d). The red and blue arrows indicate 5 d IDL of WT and drd1-6 plants, respectively. (C) Phenotypes of detached WT and drd1-6 leaves after 5-d dark incubation. (D) Photochemical efficiency of photosystem II (Fv/Fm) and (E) maximal electron transport rate (ETRmax) in WT and the drd1-6 leaves were examined at the indicated days during dark-induced senescence (DIS). Data represent average values ± SE (n = 27) of three independent experiments. * indicates P < 0.01 by student’s t-test.

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Fig 2 Expand

Fig 3.

Delayed leaf senescence symptoms in the drd1-6 mutant at later developmental stages.

Rosette leaves of 28-day-old WT and the 34, 36, and 38-day-old drd1-6 mutants were detached and darkened for 0, 3, 5 days. Photochemical efficiency of photosystem II (Fv/Fm) in WT and mutant leaves was examined at the indicated days. Data represent average values ± SE (n = 20) of independent experiments. Bars with the same letter are not significantly different at P < 0.05 by Tukey’s honestly significant difference (HSD) test.

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Fig 3 Expand

Fig 4.

Effects on chlorophyll and protein degradation in the drd1-6 plants during DIS.

(A) Chlorophyll content was measured using rosette leaves after 0d, 3 d, 5 d, and 7 d of DIS, as indicated. (B) Protein contents from the WT and the drd1-6 mutant leaves before (0 d) and after 3 d, 5 d, and 7 d of DIS. (C) Blue-Native Polyacrylamide Gel-Electrophoresis (BN-PAGE) of thylakoid protein complexes. Dodecylmaltoside-solubilized thylakoid membrane proteins corresponding to equal amounts of fresh weight were subjected to BN-PAGE. (D) Immunoblot analysis of thylakoid protein complexes. Thylakoid membranes were solubilized and subjected 15 μg of protein per well to SDS-PAGE. The band indicated by the arrow head was identified by LC MS/MS (see S2 Table). (E) D1 protein was identified by immunoblot analysis using anti-D1 antiserum.

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Fig 5.

Expression of senescence-associated genes in the drd1-6 mutant during DIS.

(A) RT-PCR and (B) Quantitative real-time PCR (qRT-PCR) analysis of gene expression in WT and the drd1-6 mutant leaves at the indicated days. SAG12, senescence-associated gene 12; ANS, antocyanidin synthase gene; CBR, chlorophyll b reductase gene; and PAO, pheophorbide α oxygenase gene. The values are normalized to ACTIN2 expression. Data indicate the mean ± SD (n = 9) of three independent experiments.

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Fig 5 Expand

Fig 6.

Transcript level changes in rosette leaves during DIS.

(A) Microarray analysis represents that the numbers of genes show two- (black), three- (gray), or fourfold (white) up- (upper) or down-(lower) regulation in expression of 0 d, 3 d, and 5 d DIS drd1-6 mutant compared to WT. (B) The number of genes with two-, three-, or fourfold increase or decrease in gene expression during 3 d and 5 d DIS compared to control (0 d) in the WT and the drd1-6 mutant are represented by black, gray, and white bars, respectively. Data represent the means of two independent Affymetrix Gene Chip analyses. FD, fold difference.

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Fig 6 Expand

Table 1.

Gene ontology analysis of differentially expressed genes (DEGs) between the WT and the drd1-6 after 5-d DIS.

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Table 1 Expand

Table 2.

Gene lists closely associated with the phenotypic differences between the WT and the drd1-6 by DIS.

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Table 2 Expand

Fig 7.

Expression of transcriptional gene silencing markers and histone methyltransferase/acetyltransferase genes in the drd1-6 mutant.

(A) Expression analysis using transcriptional gene silencing markers 180-bp centromeric repeats (CEN) and (B) transcriptionally silent information (TSI) of WT and the drd1-6 mutant during DIS. Relative RNA levels were measured by qRT-PCR and the values are normalized to ACTIN2 expression. Data indicate the mean ± SD (n = 9) from three independent experiments. Bars with the same letter are not significantly different at P < 0.05 by Tukey’s honestly significant difference (HSD) test. (C) RT-PCR analysis in the WT and the drd1-6 mutant leaves at the indicated days. SDG8, set domain group 8; SDG27, set domain protein 27; and HAC1: histone acetyltransferase of the CBP family 1. ACTIN2 was used as control. Representative data from three or more independent experiments with similar results are shown.

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Fig 8.

Delayed leaf senescence symptoms in the ddm1-2 as well as in the drd1-6 mutant.

(A) Phenotypes of detached WT, drd1-6, drd1-p and ddm1-2 leaves after 0, 3, and 5-d dark incubation. (B) Photochemical efficiency of photosystem II (Fv/Fm) in WT and mutant leaves in (A). Data represent average values ± SE (n = 27) of three independent experiments. Bars with the same letter are not significantly different at P < 0.05 by Tukey’s honestly significant difference (HSD) test.

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Fig 8 Expand