Abstract
The ancient morphoregulatory hormone auxin dynamically realigns dedicated cellular processes that shape plant growth under prevailing environmental conditions. However, the nature of the stress-responsive signal altering auxin homeostasis remains elusive. Here we establish that the evolutionarily conserved plastidial retrograde signaling metabolite methylerythritol cyclodiphosphate (MEcPP) controls adaptive growth by dual transcriptional and post-translational regulatory inputs that modulate auxin levels and distribution patterns in response to stress. We demonstrate that in vivo accumulation or exogenous application of MEcPP alters the expression of two auxin reporters, DR5:GFP and DII-VENUS, and reduces the abundance of the auxin-efflux carrier PIN-FORMED1 (PIN1) at the plasma membrane. However, pharmacological intervention with clathrin-mediated endocytosis blocks the PIN1 reduction. This study provides insight into the interplay between these two indispensable signaling metabolites by establishing the mode of MEcPP action in altering auxin homeostasis, and as such, positioning plastidial function as the primary driver of adaptive growth.
Highlights
The ancient morphoregulatory hormone auxin dynamically realigns dedicated cellular processes that shape plant growth under prevailing environmental conditions
Notable recovery of the ceh[1] short hypocotyl phenotype by exogenous application of indole-3-acetic acid (IAA) reaffirmed the involvement of this growth hormone (Fig. 1b, c)
The outcome of studies using constitutively and inducible methylerythritol cyclodiphosphate (MEcPP)-producing lines in conjunction with pharmacological interference with the methylerythritol phosphate (MEP) pathway, and with exogenous application of MEcPP, established this stress-specific plastidial retrograde signal, MEcPP, as the upstream signal defining the optimal abundance of IAA and PIN1 via dual transcriptional and posttranscriptional regulatory inputs
Summary
The ancient morphoregulatory hormone auxin dynamically realigns dedicated cellular processes that shape plant growth under prevailing environmental conditions. We establish that the evolutionarily conserved plastidial retrograde signaling metabolite methylerythritol cyclodiphosphate (MEcPP) controls adaptive growth by dual transcriptional and post-translational regulatory inputs that modulate auxin levels and distribution patterns in response to stress. Auxin metabolism is regulated by plastidial enzymes such as the plastidial NADPH-thioredoxin reductase (NTRC) This enzyme is reported to be involved in regulation of auxin levels as evidenced by reduced auxin and retarded growth of ntrc mutant as compared to the control plants[33]. These results have led to the assumption that plastidial stress-signaling metabolite(s) may play a role in maintaining auxin homeostasis and by extension regulation of plant adaptive responses. The focus on ceh[1] is because this mutant accumulates methylerythritol cyclodiphosphate (MEcPP), an essential bifunctional plastidial metabolite serving as a precursor of isoprenoids produced by the plastidial methylerythritol phosphate (MEP)
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