Abstract - Emerging evidence highlights that specific cis-carotenes may act as substrates towards the production of novel apocarotenoid signals (ACS) that regulate nuclear gene expression, metabolic homeostasis and leaf development. All cis-carotenes can accumulate in specific tissue types from Arabidopsis, rice and tomato in the absence of any carotenoid isomerase (CRTISO) activity that normally rate-limits the isomerisation of tetra-cis to all-trans-lycopene. crtiso mutants display different phenotypes in different species and the physiological basis of association with cis-carotene accumulation remains unclear. We show that cis-carotenes can accumulate in newly formed juvenile leaves of an Arabidopsis crtiso/ccr2 mutant grown under a shorter photoperiod and cause the perturbation in prolamellar body (PLB) formation as well as plastid development that delays chlorophyll biosynthesis. By way of a forward genetic screen we describe how an epistatic interaction between the ζ-carotene isomerase (ziso) and ccr2 restores PLB formation, identifying neurosporene and tetra-cis-lycopene as better substrates in the production of an ACS controlling plastid development. Transcriptomics analysis of ccr2 ziso mutant tissues impaired in plastid development revealed a signalling pathway that activates photosynthesis associated nuclear gene expression (PhANG) through the repression of DET1, thereby triggering photomorphogenesis. We next confirmed that det1 could restore PLB formation and plastid development in ccr2 tissues thereby restoring chlorophyll biosynthesis. Chemical inhibition of carotenoid cleavage dioxygenase (CCD) activity utilising the aryl-C3N hydroxamic acid analogue, D15, revealed evidence for an ACS that post-transcriptionally maintains POR protein levels and PLB formation. Four alleles of psy, a gene that encodes phytoene synthase, were identified in the forward genetic screening. The enzymatic activity of mutated PSY proteins were significantly reduced, leading to reduced cis-carotenes that may be below a threshold which triggers ACS. We showed that the interactions between PSY and ORANGE (OR) protein was diminished in ccr2 psy mutants, which consequently affected protein levels of PSY. The localization of mutated PSY proteins was not altered. In conclusion, we have identified a cis-carotene derived ACS signalling pathway that controls plastid development and signals downstream of DET1 in controlling PLB formation, plastid development and photomorphogenesis.
Biography - Dr. Xin Hou received his PhD in 2007 from the Chinese Academy of Sciences and had continued his research in Cancer Signalling until 2012. He performed Postdoctoral research on the regulatory roles of LKB1/NUAK1 signalling pathway in cancer cell proliferation and invasion, at University of Illinois from 2007 to 2009. He had then been appointed as an associate professor in China until 2012. He has started his second PhD study journey in Plant Sciences at the Australian National University since March 2012. Xin’s research has focused on apocarotenoid signals (ACSs) that regulates plant development, especially in chloroplast biogenesis.