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TCP24 modulates secondary cell wall thickening and anther endothecium development.

Wang H, Mao Y, Yang J, He Y - Front Plant Sci (2015)

Bottom Line: Several genes linked to secondary cell wall biogenesis and thickening were down-regulated in these transgenic plants.By contrast, the inhibition of TCP24 using the ectopic expression of a TCP24-SRDX repressor fusion protein, or the silencing of TCP genes by miR319a overexpression, increased cell wall lignification and the enhanced secondary cell wall thickening.Our results suggest that TCP24 acts as an important regulator of secondary cell wall thickening and modulates anther endothecium development.

View Article: PubMed Central - PubMed

Affiliation: National Key Laboratory of Plant Molecular Genetics, Shanghai Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences Shanghai, China.

ABSTRACT
miR319-targeted TCP genes are believed to regulate cell division in leaves and floral organs. However, it remains unknown whether these genes are involved in cell wall development. Here, we report that TCP24 negatively regulates secondary wall thickening in floral organs and roots. The overexpression of the miR319a-resistant version of TCP24 in Arabidopsis disrupted the thickening of secondary cell walls in the anther endothecium, leading to male sterility because of arrested anther dehiscence and pollen release. Several genes linked to secondary cell wall biogenesis and thickening were down-regulated in these transgenic plants. By contrast, the inhibition of TCP24 using the ectopic expression of a TCP24-SRDX repressor fusion protein, or the silencing of TCP genes by miR319a overexpression, increased cell wall lignification and the enhanced secondary cell wall thickening. Our results suggest that TCP24 acts as an important regulator of secondary cell wall thickening and modulates anther endothecium development.

No MeSH data available.


Related in: MedlinePlus

Phenotypes of p35S:mTCP24 plants. (A) Diagram of p35S:mTCP24 construct. (B,C) Plants of the wild type (B) and p35S:mTCP24 line (L23; C) at the rosette stage. (D,E) Plants of the wild type (D) and L23 (E) at the inflorescence stage. (F) Inflorescences of the wild type (left) and L23 plants (right). (G,H) Open flowers showing the four whorls of floral organs in the wild type (G) and L23 (H). (I,J) Anthers of the wild type (I) and L23 (J). (K) Real-time PCR analysis of TCP24 expression in the transgenic lines. Scale bars: 1 cm in (B–F); 500 μm in (G,H); 200 μm in (I,J).
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Figure 1: Phenotypes of p35S:mTCP24 plants. (A) Diagram of p35S:mTCP24 construct. (B,C) Plants of the wild type (B) and p35S:mTCP24 line (L23; C) at the rosette stage. (D,E) Plants of the wild type (D) and L23 (E) at the inflorescence stage. (F) Inflorescences of the wild type (left) and L23 plants (right). (G,H) Open flowers showing the four whorls of floral organs in the wild type (G) and L23 (H). (I,J) Anthers of the wild type (I) and L23 (J). (K) Real-time PCR analysis of TCP24 expression in the transgenic lines. Scale bars: 1 cm in (B–F); 500 μm in (G,H); 200 μm in (I,J).

Mentions: Mutations in single CIN-like TCP genes do not generate visible phenotypes owing to the redundancy among these genes (Koyama et al., 2007). To characterize the role of TCP24 during plant development, we first constructed mTCP24, the miR319a-resistant version of TCP24, which contains nucleotide substitutions in the miR319a-binding region that do not change the encoded amino acid sequence (Figure 1A), as they did for mTCP2, mTCP3, and mTCP4 (Palatnik et al., 2003; Koyama et al., 2007). In the p35S:mTCP24 plants, the rosette leaves were turned slightly downward (Figures 1B,C), the number of branches increased compared with the wild type (Figures 1D,E), and importantly, the flowers were partially or completely sterile (Figure 1F). Under optical microscopy, anther dehiscence was arrested (Figures 1G–J), albeit to different extents between the transgenic lines. Transcripts of TCP24 were elevated in these independent transgenic lines compared with wild type (Figure 1K). Among these transgenic lines, the higher the TCP24 expression was, the higher the male sterility was, indicating a correlation between the expression levels of TCP24 and the severity of the sterile phenotypes (Supplementary Figure S1). The L2 and L23, two completely sterile lines, set seeds when they were pollinated with the wild type pollen, indicating that p35S:mTCP24 did not affect female fertility.


TCP24 modulates secondary cell wall thickening and anther endothecium development.

Wang H, Mao Y, Yang J, He Y - Front Plant Sci (2015)

Phenotypes of p35S:mTCP24 plants. (A) Diagram of p35S:mTCP24 construct. (B,C) Plants of the wild type (B) and p35S:mTCP24 line (L23; C) at the rosette stage. (D,E) Plants of the wild type (D) and L23 (E) at the inflorescence stage. (F) Inflorescences of the wild type (left) and L23 plants (right). (G,H) Open flowers showing the four whorls of floral organs in the wild type (G) and L23 (H). (I,J) Anthers of the wild type (I) and L23 (J). (K) Real-time PCR analysis of TCP24 expression in the transgenic lines. Scale bars: 1 cm in (B–F); 500 μm in (G,H); 200 μm in (I,J).
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
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Figure 1: Phenotypes of p35S:mTCP24 plants. (A) Diagram of p35S:mTCP24 construct. (B,C) Plants of the wild type (B) and p35S:mTCP24 line (L23; C) at the rosette stage. (D,E) Plants of the wild type (D) and L23 (E) at the inflorescence stage. (F) Inflorescences of the wild type (left) and L23 plants (right). (G,H) Open flowers showing the four whorls of floral organs in the wild type (G) and L23 (H). (I,J) Anthers of the wild type (I) and L23 (J). (K) Real-time PCR analysis of TCP24 expression in the transgenic lines. Scale bars: 1 cm in (B–F); 500 μm in (G,H); 200 μm in (I,J).
Mentions: Mutations in single CIN-like TCP genes do not generate visible phenotypes owing to the redundancy among these genes (Koyama et al., 2007). To characterize the role of TCP24 during plant development, we first constructed mTCP24, the miR319a-resistant version of TCP24, which contains nucleotide substitutions in the miR319a-binding region that do not change the encoded amino acid sequence (Figure 1A), as they did for mTCP2, mTCP3, and mTCP4 (Palatnik et al., 2003; Koyama et al., 2007). In the p35S:mTCP24 plants, the rosette leaves were turned slightly downward (Figures 1B,C), the number of branches increased compared with the wild type (Figures 1D,E), and importantly, the flowers were partially or completely sterile (Figure 1F). Under optical microscopy, anther dehiscence was arrested (Figures 1G–J), albeit to different extents between the transgenic lines. Transcripts of TCP24 were elevated in these independent transgenic lines compared with wild type (Figure 1K). Among these transgenic lines, the higher the TCP24 expression was, the higher the male sterility was, indicating a correlation between the expression levels of TCP24 and the severity of the sterile phenotypes (Supplementary Figure S1). The L2 and L23, two completely sterile lines, set seeds when they were pollinated with the wild type pollen, indicating that p35S:mTCP24 did not affect female fertility.

Bottom Line: Several genes linked to secondary cell wall biogenesis and thickening were down-regulated in these transgenic plants.By contrast, the inhibition of TCP24 using the ectopic expression of a TCP24-SRDX repressor fusion protein, or the silencing of TCP genes by miR319a overexpression, increased cell wall lignification and the enhanced secondary cell wall thickening.Our results suggest that TCP24 acts as an important regulator of secondary cell wall thickening and modulates anther endothecium development.

View Article: PubMed Central - PubMed

Affiliation: National Key Laboratory of Plant Molecular Genetics, Shanghai Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences Shanghai, China.

ABSTRACT
miR319-targeted TCP genes are believed to regulate cell division in leaves and floral organs. However, it remains unknown whether these genes are involved in cell wall development. Here, we report that TCP24 negatively regulates secondary wall thickening in floral organs and roots. The overexpression of the miR319a-resistant version of TCP24 in Arabidopsis disrupted the thickening of secondary cell walls in the anther endothecium, leading to male sterility because of arrested anther dehiscence and pollen release. Several genes linked to secondary cell wall biogenesis and thickening were down-regulated in these transgenic plants. By contrast, the inhibition of TCP24 using the ectopic expression of a TCP24-SRDX repressor fusion protein, or the silencing of TCP genes by miR319a overexpression, increased cell wall lignification and the enhanced secondary cell wall thickening. Our results suggest that TCP24 acts as an important regulator of secondary cell wall thickening and modulates anther endothecium development.

No MeSH data available.


Related in: MedlinePlus