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Overexpression of AtBMI1C, a polycomb group protein gene, accelerates flowering in Arabidopsis.

Li W, Wang Z, Li J, Yang H, Cui S, Wang X, Ma L - PLoS ONE (2011)

Bottom Line: No change in the H3K27me3 level in FLC chromatin was detected in an AtBMI1C-overexpressing line.Our results suggest that AtBMI1C participates in flowering time control by regulating the expression of FLC; moreover, the repression of FLC by AtBMI1C is not due to the activity of PRC2.Instead, it is likely the result of PRC1 activity, into which AtBMI1C is integrated.

View Article: PubMed Central - PubMed

Affiliation: Hebei Key Laboratory of Molecular Cell Biology, College of Biological Sciences, Hebei Normal University, Shijiazhuang, Hebei, China.

ABSTRACT
Polycomb group protein (PcG)-mediated gene silencing is emerging as an essential developmental regulatory mechanism in eukaryotic organisms. PcGs inactivate or maintain the silenced state of their target chromatin by forming complexes, including Polycomb Repressive Complex 1 (PRC1) and 2 (PRC2). Three PRC2 complexes have been identified and characterized in Arabidopsis; of these, the EMF and VRN complexes suppress flowering by catalyzing the trimethylation of lysine 27 on histone H3 of FLOWER LOCUS T (FT) and FLOWER LOCUS C (FLC). However, little is known about the role of PRC1 in regulating the floral transition, although AtRING1A, AtRING1B, AtBMI1A, and AtBMI1B are believed to regulate shoot apical meristem and embryonic development as components of PRC1. Moreover, among the five RING finger PcGs in the Arabidopsis genome, four have been characterized. Here, we report that the fifth, AtBMI1C, is a novel, ubiquitously expressed nuclear PcG protein and part of PRC1, which is evolutionarily conserved with Psc and BMI1. Overexpression of AtBMI1C caused increased H2A monoubiquitination and flowering defects in Arabidopsis. Both the suppression of FLC and activation of FT were observed in AtBMI1C-overexpressing lines, resulting in early flowering. No change in the H3K27me3 level in FLC chromatin was detected in an AtBMI1C-overexpressing line. Our results suggest that AtBMI1C participates in flowering time control by regulating the expression of FLC; moreover, the repression of FLC by AtBMI1C is not due to the activity of PRC2. Instead, it is likely the result of PRC1 activity, into which AtBMI1C is integrated.

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Identification of the AtBMI1C mutant and characterization of artificial microRNAi lines.(A) Genomic architecture of AtBMI1C and position of the mutation in atbmi1c-1. The 5′ or 3′ UTR is represented by a gray bar. Exons are represented by black bars. Introns are represented by black lines. The T-DNA insertion in atbmi1c-1 (SALK_148143) is located in the 5′ UTR of AtBMI1C. Scale bar, 500 bp. (B) Detection of AtBMI1C mRNA in a homozygous atbmi1c-1 T-DNA insertion line by semiquantitative RT-PCR. Total RNA was extracted from the inflorescences of homozygous atbmi1c and wild-type plants. Semiquantitative RT-PCR was performed to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (C) Characterization of AtBMI1C mRNA abundance in AtBMI1C-Rs. Total RNA was extracted from the inflorescences of AtBMI1C-Rs and wild-type plants. Semiquantitative RT-PCR was conducted to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (D) Morphology of the AtBMI1C-Rs, in which AtBMI1C was down-regulated, compared to wild type and AtBMI1C-R12, an amiRNAi line in which the expression of AtBMI1C was almost the same as in wild type. (E) Flowering time in the AtBMI1C-Rs was the same as in wild type. Plants were grown under LD conditions. The number of rosette leaves was determined after bolting.
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pone-0021364-g004: Identification of the AtBMI1C mutant and characterization of artificial microRNAi lines.(A) Genomic architecture of AtBMI1C and position of the mutation in atbmi1c-1. The 5′ or 3′ UTR is represented by a gray bar. Exons are represented by black bars. Introns are represented by black lines. The T-DNA insertion in atbmi1c-1 (SALK_148143) is located in the 5′ UTR of AtBMI1C. Scale bar, 500 bp. (B) Detection of AtBMI1C mRNA in a homozygous atbmi1c-1 T-DNA insertion line by semiquantitative RT-PCR. Total RNA was extracted from the inflorescences of homozygous atbmi1c and wild-type plants. Semiquantitative RT-PCR was performed to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (C) Characterization of AtBMI1C mRNA abundance in AtBMI1C-Rs. Total RNA was extracted from the inflorescences of AtBMI1C-Rs and wild-type plants. Semiquantitative RT-PCR was conducted to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (D) Morphology of the AtBMI1C-Rs, in which AtBMI1C was down-regulated, compared to wild type and AtBMI1C-R12, an amiRNAi line in which the expression of AtBMI1C was almost the same as in wild type. (E) Flowering time in the AtBMI1C-Rs was the same as in wild type. Plants were grown under LD conditions. The number of rosette leaves was determined after bolting.

Mentions: To investigate the biological function of AtBMI1C in Arabidopsis, T-DNA insertion mutants of AtBMI1C were ordered from the Arabidopsis Biological Resource Center (ABRC). A homozygous T-DNA insertion allele of AtBMI1C was identified (Atbmi1c-1, SALK_148143), in which the T-DNA was inserted upstream of the start codon (Figure 4A). However, the T-DNA insertion in Atbmi1c-1 did not abolish the expression of AtBMI1C (Figure 4B). Not surprisingly, no visible phenotype was detected among the homozygous mutant plants (data not shown).


Overexpression of AtBMI1C, a polycomb group protein gene, accelerates flowering in Arabidopsis.

Li W, Wang Z, Li J, Yang H, Cui S, Wang X, Ma L - PLoS ONE (2011)

Identification of the AtBMI1C mutant and characterization of artificial microRNAi lines.(A) Genomic architecture of AtBMI1C and position of the mutation in atbmi1c-1. The 5′ or 3′ UTR is represented by a gray bar. Exons are represented by black bars. Introns are represented by black lines. The T-DNA insertion in atbmi1c-1 (SALK_148143) is located in the 5′ UTR of AtBMI1C. Scale bar, 500 bp. (B) Detection of AtBMI1C mRNA in a homozygous atbmi1c-1 T-DNA insertion line by semiquantitative RT-PCR. Total RNA was extracted from the inflorescences of homozygous atbmi1c and wild-type plants. Semiquantitative RT-PCR was performed to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (C) Characterization of AtBMI1C mRNA abundance in AtBMI1C-Rs. Total RNA was extracted from the inflorescences of AtBMI1C-Rs and wild-type plants. Semiquantitative RT-PCR was conducted to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (D) Morphology of the AtBMI1C-Rs, in which AtBMI1C was down-regulated, compared to wild type and AtBMI1C-R12, an amiRNAi line in which the expression of AtBMI1C was almost the same as in wild type. (E) Flowering time in the AtBMI1C-Rs was the same as in wild type. Plants were grown under LD conditions. The number of rosette leaves was determined after bolting.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3119047&req=5

pone-0021364-g004: Identification of the AtBMI1C mutant and characterization of artificial microRNAi lines.(A) Genomic architecture of AtBMI1C and position of the mutation in atbmi1c-1. The 5′ or 3′ UTR is represented by a gray bar. Exons are represented by black bars. Introns are represented by black lines. The T-DNA insertion in atbmi1c-1 (SALK_148143) is located in the 5′ UTR of AtBMI1C. Scale bar, 500 bp. (B) Detection of AtBMI1C mRNA in a homozygous atbmi1c-1 T-DNA insertion line by semiquantitative RT-PCR. Total RNA was extracted from the inflorescences of homozygous atbmi1c and wild-type plants. Semiquantitative RT-PCR was performed to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (C) Characterization of AtBMI1C mRNA abundance in AtBMI1C-Rs. Total RNA was extracted from the inflorescences of AtBMI1C-Rs and wild-type plants. Semiquantitative RT-PCR was conducted to amplify the full-length transcript using ACTIN2/7 as an endogenous control. (D) Morphology of the AtBMI1C-Rs, in which AtBMI1C was down-regulated, compared to wild type and AtBMI1C-R12, an amiRNAi line in which the expression of AtBMI1C was almost the same as in wild type. (E) Flowering time in the AtBMI1C-Rs was the same as in wild type. Plants were grown under LD conditions. The number of rosette leaves was determined after bolting.
Mentions: To investigate the biological function of AtBMI1C in Arabidopsis, T-DNA insertion mutants of AtBMI1C were ordered from the Arabidopsis Biological Resource Center (ABRC). A homozygous T-DNA insertion allele of AtBMI1C was identified (Atbmi1c-1, SALK_148143), in which the T-DNA was inserted upstream of the start codon (Figure 4A). However, the T-DNA insertion in Atbmi1c-1 did not abolish the expression of AtBMI1C (Figure 4B). Not surprisingly, no visible phenotype was detected among the homozygous mutant plants (data not shown).

Bottom Line: No change in the H3K27me3 level in FLC chromatin was detected in an AtBMI1C-overexpressing line.Our results suggest that AtBMI1C participates in flowering time control by regulating the expression of FLC; moreover, the repression of FLC by AtBMI1C is not due to the activity of PRC2.Instead, it is likely the result of PRC1 activity, into which AtBMI1C is integrated.

View Article: PubMed Central - PubMed

Affiliation: Hebei Key Laboratory of Molecular Cell Biology, College of Biological Sciences, Hebei Normal University, Shijiazhuang, Hebei, China.

ABSTRACT
Polycomb group protein (PcG)-mediated gene silencing is emerging as an essential developmental regulatory mechanism in eukaryotic organisms. PcGs inactivate or maintain the silenced state of their target chromatin by forming complexes, including Polycomb Repressive Complex 1 (PRC1) and 2 (PRC2). Three PRC2 complexes have been identified and characterized in Arabidopsis; of these, the EMF and VRN complexes suppress flowering by catalyzing the trimethylation of lysine 27 on histone H3 of FLOWER LOCUS T (FT) and FLOWER LOCUS C (FLC). However, little is known about the role of PRC1 in regulating the floral transition, although AtRING1A, AtRING1B, AtBMI1A, and AtBMI1B are believed to regulate shoot apical meristem and embryonic development as components of PRC1. Moreover, among the five RING finger PcGs in the Arabidopsis genome, four have been characterized. Here, we report that the fifth, AtBMI1C, is a novel, ubiquitously expressed nuclear PcG protein and part of PRC1, which is evolutionarily conserved with Psc and BMI1. Overexpression of AtBMI1C caused increased H2A monoubiquitination and flowering defects in Arabidopsis. Both the suppression of FLC and activation of FT were observed in AtBMI1C-overexpressing lines, resulting in early flowering. No change in the H3K27me3 level in FLC chromatin was detected in an AtBMI1C-overexpressing line. Our results suggest that AtBMI1C participates in flowering time control by regulating the expression of FLC; moreover, the repression of FLC by AtBMI1C is not due to the activity of PRC2. Instead, it is likely the result of PRC1 activity, into which AtBMI1C is integrated.

Show MeSH
Related in: MedlinePlus