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Plant J ; 118(1): 141-158, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38128030

RESUMEN

The development of photosynthetically competent seedlings requires both light and retrograde biogenic signaling pathways. The transcription factor GLK1 functions at the interface between these pathways and receives input from the biogenic signal integrator GUN1. BBX14 was previously identified, together with GLK1, in a core module that mediates the response to high light (HL) levels and biogenic signals, which was studied by using inhibitors of chloroplast development. Our chromatin immunoprecipitation-Seq experiments revealed that BBX14 is a direct target of GLK1, and RNA-Seq analysis suggests that BBX14 may function as a regulator of the circadian clock. In addition, BBX14 plays a role in chlorophyll biosynthesis during early onset of light. Knockout of BBX14 results in a long hypocotyl phenotype dependent on a retrograde signal. Furthermore, the expression of BBX14 and BBX15 during biogenic signaling requires GUN1. Investigation of the role of BBX14 and BBX15 in GUN-type biogenic (gun) signaling showed that the overexpression of BBX14 or BBX15 caused de-repression of CA1 mRNA levels, when seedlings were grown on norflurazon. Notably, transcripts of the LHCB1.2 marker are not de-repressed. Furthermore, BBX14 is required to acclimate plants to HL stress. We propose that BBX14 is an integrator of biogenic signals and that BBX14 is a nuclear target of retrograde signals downstream of the GUN1/GLK1 module. However, we do not classify BBX14 or BBX15 overexpressors as gun mutants based on a critical evaluation of our results and those reported in the literature. Finally, we discuss a classification system necessary for the declaration of new gun mutants.


Asunto(s)
Proteínas de Arabidopsis , Arabidopsis , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Proteínas de Unión al ADN/genética , Regulación de la Expresión Génica de las Plantas , Plantones/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo
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