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Chloroplast retrograde signal regulates flowering

Proper timing of flowering transition is vital for the reproductive success of plants and orchestrated by endogenous and external factors; however, the mechanisms of how plants regulate flowering under high light are not well understood. In this study, we show that promotion of flowering by high light involves the coupling of chloroplast retrograde signals and transcriptional silencing of the floral repressor FLOWERING LOCUS C (FLC).

Peiqiang Feng, Hailong Guo, Wei Chi, Xin Chai, Xuwu Sun, Xiumei Xu, Jinfang Ma, Jean-David Rochaix, Dario Leister, Haiyang Wang, Congming Lu, and Lixin Zhang

Significance

Proper timing of flowering transition is vital for the reproductive success of plants and orchestrated by endogenous and external factors; however, the mechanisms of how plants regulate flowering under high light are not well understood. In this study, we show that promotion of flowering by high light involves the coupling of chloroplast retrograde signals and transcriptional silencing of the floral repressor FLOWERING LOCUS C (FLC). In response to high light, a chloroplast envelope-localized transcription factor, PTM, releases its N-terminal fragment through processing to associate with the chromatin remodeler FVE and suppresses FLC transcription. This report describes the molecular basis for a unique intracellular signaling pathway derived from chloroplasts in which plants regulate the developmental timing of the flowering transition.

Abstract

Light is a major environmental factor regulating flowering time, thus ensuring reproductive success of higher plants. In contrast to our detailed understanding of light quality and photoperiod mechanisms involved, the molecular basis underlying high light-promoted flowering remains elusive. Here we show that, in Arabidopsis, a chloroplast-derived signal is critical for high light-regulated flowering mediated by the FLOWERING LOCUS C (FLC). We also demonstrate that PTM, a PHD transcription factor involved in chloroplast retrograde signaling, perceives such a signal and mediates transcriptional repression of FLC through recruitment of FVE, a component of the histone deacetylase complex. Thus, our data suggest that chloroplasts function as essential sensors of high light to regulate flowering and adaptive responses by triggering nuclear transcriptional changes at the chromatin level.

 

See: http://www.pnas.org/content/113/38/10708.abstract.html?etoc

PNAS September 20 2016; vol.113; no.38: 10708–10713

 

Fig. 1.

FLC is required for high light-induced flowering in Arabidopsis. (A) Images of WT plants showing their flowering phenotype under different light irradiances (300, 500, and 800 μmol m−2 s−1). CK represents normal light (100 μmol m−2 s−1). (B) Flowering times of WT plants under different light irradiances assessed by leaf number. Red bars represent cauline leaves, and blue bars represent rosette leaves. Total leaf numbers were counted using at least 16 plants. (C) Flowering times of Col-0, flc-3, and the complemented plants under normal light (100 μmol m−2 s−1) and high light (800 μmol m−2 s−1). CK, normal light; HL, high light. (D) Effects of high light treatment on FLC expression. Plants treated with different light intensities (Left) under LD (16-h light/8-h dark) conditions were used for extraction of total RNA, and mRNA levels of FLC were determined using qRT-PCR. Values shown are mean ± SD; n = 3. The results were statistically treated using Student’s t test. *P < 0.05; **P < 0.01; ns, not significant.

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