4.8 Article

Phytochrome and retrograde signalling pathways converge to antagonistically regulate a light-induced transcriptional network

Journal

NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms11431

Keywords

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Funding

  1. Spanish 'Ministerio de Ciencia e Innovacion' [BIO2009-07675]
  2. Ministerio de Economia [BIO2012-31672, BIO2012-31860]
  3. Ministerio de Educacion, Cultura y Deporte [PRX12/00631]
  4. Generalitat de Catalunya [2009-SGR-206]
  5. 'Comissionat per a Universitats i Recerca del Departament d'Innovacio, Universitats i Empresa' fellowship from the Generalitat de Catalunya (Beatriu de Pinos programme)
  6. Marie Curie IRG grant [PIRG06-GA-2009-256420]
  7. National Institutes of Health (NIH) [2R01 GM-047475]
  8. USDA ARS Current Research Information System [5335-21000-032-00D]

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Plastid-to-nucleus retrograde signals emitted by dysfunctional chloroplasts impact photomorphogenic development, but the molecular link between retrograde-and photosensory-receptor signalling has remained unclear. Here, we show that the phytochrome and retrograde signalling (RS) pathways converge antagonistically to regulate the expression of the nuclear-encoded transcription factor GLK1, a key regulator of a light-induced transcriptional network central to photomorphogenesis. GLK1 gene transcription is directly repressed by PHYTOCHROME-INTERACTING FACTOR (PIF)-class bHLH transcription factors in darkness, but light-activated phytochrome reverses this activity, thereby inducing expression. Conversely, we show that retrograde signals repress this induction by a mechanism independent of PIF mediation. Collectively, our data indicate that light at moderate levels acts through the plant's nuclear-localized sensory-photoreceptor system to induce appropriate photomorphogenic development, but at excessive levels, sensed through the separate plastid-localized RS system, acts to suppress such development, thus providing a mechanism for protection against photo-oxidative damage by minimizing the tissue exposure to deleterious radiation.

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