# Coordinated cpSRP43 and cpSRP54 Abundance Is Essential for Tetrapyrrole Biosynthesis While cpSRP43 Is Independent of Retrograde Signaling

## TL;DR

The study shows that cpSRP43 and cpSRP54 work together for chloroplast function and pigment production, but cpSRP43 doesn't send signals to the plant's nucleus.

## Contribution

The coordinated regulation of cpSRP43 and cpSRP54 is essential for tetrapyrrole biosynthesis, and cpSRP43 is independent of retrograde signaling.

## Key findings

- cpSRP43 and cpSRP54 levels are interdependently controlled, affecting chloroplast function and tetrapyrrole biosynthesis.
- cpSRP43 deficiency worsens the pale-green phenotype in gun4 and gun5 mutants, but overexpression doesn't rescue these defects.
- cpSRP43 does not participate in plastid-to-nucleus retrograde signaling under intrinsic plastid stress.

## Abstract

The chloroplast signal recognition particle (cpSRP) components cpSRP43 and cpSRP54 not only form a complex with light-harvesting chlorophyll (Chl)-binding proteins to direct them to the thylakoid membrane, but also serve other functions. cpSRP43 independently acts as a chaperone for some tetrapyrrole biosynthesis (TBS) enzymes, while cpSRP54 participates in the co-translational targeting of plastid-encoded proteins. However, it remains unclear to what extent the two cpSRP components are coregulated—despite their distinct functions—and whether both participate in genomes-uncoupled (GUN)-mediated retrograde signaling. Here, we demonstrate that cpSRP43 and cpSRP54 accumulation is strongly interdependently controlled: overexpression of one protein increases the level of the other, while a deficiency in one of the two proteins leads to a simultaneous decrease in the other component. Disruption of this balance, e.g., by combining the overexpression of one component with a knockout of the other, results in severe chlorosis, stunted growth, and reduced levels of Chl and tetrapyrrole intermediates. Moreover, cpSRP43 deficiency exacerbates the pale-green phenotype of gun4 and gun5 mutants, highlighting a synergistic impact on TBS; however, cpSRP43 overexpression fails to rescue these defects. Remarkably, loss of cpSRP43 does not affect the expression of nuclear-encoded photosynthetic genes under intrinsic plastid stress, clearly demonstrating that cpSRP43 is not involved in plastid-to-nucleus retrograde signaling. Overall, our findings underscore that the fine-tuned expression of cpSRP43 and cpSRP54 is crucial for proper chloroplast function and pigment biosynthesis, while cpSRP43 alone does not participate in the retrograde signaling pathway.