Too Much, Take it Back: PAP Moves from the Cytosol to Plastids and Mitochondria for Degradation via PAPST2

Tee, Estee E-Ling

doi:10.1105/tpc.18.00944

Cited by 1 publication

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“…The subcellular localization of its components is important for the function of the SAL1-PAP pathway in retrograde signaling (Figure 1). As the precursor of PAP, 3′phosphoadenosine 5′-phosphosulfate (PAPS) is mainly synthesized in chloroplasts and transported into the cytosol by PAPST1 (Gigolashvili et al, 2012) and, to a lesser extent, by PAPST2 (Tee, 2018;Ashykhmina et al, 2019), where it is used as a sulfate donor by sulfotransferases (SOTs) for various sulfation reactions. These reactions generate PAP in the cytosol, which is then transported into chloroplasts and the mitochondria for degradation by SAL1 (Estavillo et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Dissecting the Role of SAL1 in Metabolizing the Stress Signaling Molecule 3′-Phosphoadenosine 5′-Phosphate in Different Cell Compartments

Ashykhmina

Chan

Frerigmann

et al. 2022

Front. Mol. Biosci.

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Plants possess the most highly compartmentalized eukaryotic cells. To coordinate their intracellular functions, plastids and the mitochondria are dependent on the flow of information to and from the nuclei, known as retrograde and anterograde signals. One mobile retrograde signaling molecule is the monophosphate 3′-phosphoadenosine 5′-phosphate (PAP), which is mainly produced from 3′-phosphoadenosine 5′-phosphosulfate (PAPS) in the cytosol and regulates the expression of a set of nuclear genes that modulate plant growth in response to biotic and abiotic stresses. The adenosine bisphosphate phosphatase enzyme SAL1 dephosphorylates PAP to AMP in plastids and the mitochondria, but can also rescue sal1 Arabidopsis phenotypes (PAP accumulation, leaf morphology, growth, etc.) when expressed in the cytosol and the nucleus. To understand better the roles of the SAL1 protein in chloroplasts, the mitochondria, nuclei, and the cytosol, we have attempted to complement the sal1 mutant by specifically cargoing the transgenic SAL1 protein to these four cell compartments. Overexpression of SAL1 protein targeted to the nucleus or the mitochondria alone, or co-targeted to chloroplasts and the mitochondria, complemented most aspects of the sal1 phenotypes. Notably, targeting SAL1 to chloroplasts or the cytosol did not effectively rescue the sal1 phenotypes as these transgenic lines accumulated very low levels of SAL1 protein despite overexpressing SAL1 mRNA, suggesting a possibly lower stability of the SAL1 protein in these compartments. The diverse transgenic SAL1 lines exhibited a range of PAP levels. The latter needs to reach certain thresholds in the cell for its impacts on different processes such as leaf growth, regulation of rosette morphology, sulfate homeostasis, and glucosinolate biosynthesis. Collectively, these findings provide an initial platform for further dissection of the role of the SAL1–PAP pathway in different cellular processes under stress conditions.

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