Autophagy mutants show delayed chloroplast development during de‐etiolation in carbon limiting conditions
0301 basic medicine
2. Zero hunger
Chloroplasts
Light
Arabidopsis Proteins
Arabidopsis
Autophagy-Related Proteins
Membrane Transport Proteins
Darkness
Lipid Metabolism
Aminopeptidases
Carbon
03 medical and health sciences
Gene Expression Regulation, Plant
Seedlings
Etiolation
Mutation
Autophagy
Photosynthesis
Carboxylic Ester Hydrolases
DOI:
10.1111/tpj.15452
Publication Date:
2021-08-08T16:57:38Z
AUTHORS (9)
ABSTRACT
SUMMARYAutophagy is a conserved catabolic process that plays an essential role under nutrient starvation conditions and influences different developmental processes. We observed that seedlings of autophagy mutants (atg2, atg5, atg7, and atg9) germinated in the dark showed delayed chloroplast development following illumination. The delayed chloroplast development was characterized by a decrease in photosynthetic and chlorophyll biosynthetic proteins, lower chlorophyll content, reduced chloroplast size, and increased levels of proteins involved in lipid biosynthesis. Confirming the biological impact of these differences, photosynthetic performance was impaired in autophagy mutants 12 h post‐illumination. We observed that while gene expression for photosynthetic machinery during de‐etiolation was largely unaffected in atg mutants, several genes involved in photosystem assembly were transcriptionally downregulated. We also investigated if the delayed chloroplast development could be explained by lower lipid import to the chloroplast or lower triglyceride (TAG) turnover. We observed that the limitations in the chloroplast lipid import imposed by trigalactosyldiacylglycerol1 are unlikely to explain the delay in chloroplast development. However, we found that lower TAG mobility in the triacylglycerol lipase mutant sugardependent1 significantly affected de‐etiolation. Moreover, we showed that lower levels of carbon resources exacerbated the slow greening phenotype whereas higher levels of carbon resources had an opposite effect. This work suggests a lack of autophagy machinery limits chloroplast development during de‐etiolation, and this is exacerbated by limited lipid turnover (lipophagy) that physically or energetically restrains chloroplast development.
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