S. Y. Phua
Dec 2, 2015
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Abstract
3’-phosphoadenosine 5’-phosphate (PAP) was recently proposed as a new chloroplast retrograde signal that accumulates during drought stress. PAP is a by-product of secondary sulfur assimilation, generated by SULFOTRANSFERASES (SOTs) upon transferring of the sulfate group from 3’-phosphoadenosine 5’-phosphosulfate (PAPS) to sulfate acceptor molecules. PAP is efficiently degraded by the SAL1 phosphatase into inorganic phosphate and adenosine monophosphate (AMP). Consequently, PAP levels are normally kept at very low during plant development. Constitutive over-accumulation of this retrograde signal resulted in plants with pleiotropic altered phenotypes as demonstrated by the sal1 mutant in Arabidopsis, namely improved drought tolerance, altered rosette morphology and delayed development. These multifaceted altered phenotypes of sal1 correlate well with the many transcriptional changes, which are mainly due to the inhibition of 5’3’ EXORIBONUCLEASES (XRNs) by PAP. However, the details of downstream changes that links SAL1-PAP-XRN to the many altered phenotypes of sal1 remains poorly understood. This thesis investigates the possibility of conferring drought tolerance to plants by manipulating the SAL1 gene expression with minimal negative effects on growth, while unraveling the signalling pathway(s) contributing to sal1 altered development and drought tolerance. I hypothesised that PAP accumulation at early developmental stages is detrimental for plant growth and development while its accumulation at later stages of development or prior to drought stress is beneficiary for conferring plant drought tolerance. To test this hypothesis, two different strategies for easy manipulation of SAL1 expression were attempted: inducible silencing of SAL1 in wild-type Arabidopsis and inducible complementation of SAL1 in the sal1 mutant background. Surprisingly, efficient silencing of SAL1 could not be achieved even with a strong constitutive promoter driving the expression of SAL1-hair-pin RNA interference (hpRNAi) or SAL1-artificial microRNA (amiRNA) and inducible-silencing was similarly inefficient. On the other hand, inducible complementation of SAL1 in the sal1 mutant background allowed for better manipulation of SAL1 expression and PAP