ArticlebioRxiv : the preprint server for biology2025
Chemical modulation of chloroplast de- and re-differentiation reveals a role for the SAL1-PAP retrograde pathway in facilitating plastid transitions.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Plastids are dynamic organelles that remodel their composition, ultrastructure, and function according to developmental and environmental demands. The synthetic molecule X57 induces the conversion of leaf chloroplasts into tocopherol-rich plastids lacking thylakoids and containing proliferating plastoglobules. Removal of X57 triggers chloroplast re-differentiation, enabling precise spatial-temporal dissection of these transitions. X57 directly binds and inhibits the phosphatase SAL1, causing accumulation of its substrate 3'-phosphoadenosine 5'-phosphate (PAP), a retrograde signal that modulates nuclear gene expression. SAL1 inhibition and subsequent PAP accumulation activate a cascade that depletes cytokinins and down-regulates GOLDEN2-LIKE1 (GLK1) and other transcription factors involved in chloroplast biogenesis. SAL1-defective mutants fail to undergo this signaling pathway. The SAL1-PAP-mediated weakening of chloroplast identity preconditions plastids for their eventual conversion into storage-type organelles upon X57-promoted accumulation of tocopherols. After X57 withdrawal, photosynthetic gene expression and chloroplast functions are restored. This framework identifies key molecular mechanisms underlying chloroplast plasticity, a central process in biology.
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