A mixed selection of research in this UK Arabidopsis Roundup. Firstly a study from Stefan Kepinski and Mark Estelle that adds another layer of understanding to the regulation of the auxin response. Enrique Lopez-Juez leads a study into signaling between the nucleus and chloroplast while Tracey Lawson contributes to an investigation into role of starch metabolism in guard cells. Fran Maathuis and co-worker looks at differences in vacuolar transport between Arabidopsis ecotypes while Alan Marchant is involved in a study of cell wall pectins. Finally William Amos has uses the 1001genomes project to investigate heterozygote instability (HI).
Wang R, Zhang Y, Kieffer M, Yu H, Kepinski S, Estelle M (2016) HSP90 regulates temperature-dependent seedling growth in Arabidopsis by stabilizing the auxin co-receptor F-box protein TIR1. Nat Commun. 5;7:10269. http://dx.doi.org/10.1038/ncomms10269 Open Access
Stefan Kepinski (Leeds) is the UK lead on this collaboration with Mark Estelle from UCSD and it continues their previous work that investigates the much-studied auxin receptor TIR1. Arabidopsis seedlings grown at 29C show auxin-dependent hypocotyl elongation although the molecular mechanism behind this response has remained opaque. In this study they show that in high temperatures TIR1 accumulates in a manner dependent on the molecular chaperone, HSP90. In addition HSP90 and the co-chaperone SGT1 directly interact with TIR1. Inhibition of HSP90 results in degradation of the TIR1 and causes a range of auxin-mediated growth processes at both high and low temperatures. This study adds another level of complexity to the molecular basis of the auxin response.
Hills AC, Khan S, López-Juez E (2015) Chloroplast Biogenesis-Associated Nuclear Genes: Control by Plastid Signals Evolved Prior to Their Regulation as Part of Photomorphogenesis. Front Plant Sci. 10;6:1078. http://dx.doi.org/10.3389/fpls.2015.01078 Open Access
The work comes exclusively from the lab of Enrique Lopez-Juez at Royal Holloway and investigates at the expression of photosynthesis-associated nuclear genes (PhANGs). This expression is dependent on light as well as plastid-to-nucleus “biogenic” communication signals and causes the assembly of photosynthesis component chloroplasts. The authors investigate the factors that control the activity of the Lhcb promotor in the light and the dark, both in angiosperms and gymnosperms. They propose that suppression of PhANG responses has contributed to the evolution of light-controlled chloroplast biogenesis.
Horrer D, Flütsch S, Pazmino D, Matthews JS, Thalmann M, Nigro A, Leonhardt N, Lawson T, Santelia D (2015) Blue Light Induces a Distinct Starch Degradation Pathway in Guard Cells for Stomatal Opening. Current Biology http://dx.doi.org/10.1016/j.cub.2015.12.036
Tracey Lawson (University of Essex) is the UK lead on this UK-French-Swiss study that uses the stomatal guard cell experimental system to investigate the role of carbon metabolism in the response to blue light. Interestingly guard cells differ from other leave tissues in that they contain starch at the end of the night. However this starch store is rapidly degraded within 30minutes of light and is important for stomatal opening and subsequent biomass production. This starch degradation involves action of two enzymes, β-amylase 1 (BAM1) and α-amylase 3 (AMY3) that do not function during night time starch degradation in other tissues. This process is coordinated by blue light signalling and correlates with the activity of a plasma membrane ATPase. This study adds yet another level of our understanding into the mechanism of stomatal opening. See image for a proposed model of this process (from Cell Press).
Hartley TN, Maathuis FJ (2015) Allelic variation in the vacuolar TPK1 channel affects its calcium dependence and may impact on stomatal conductance. FEBS Lett. 90(1):110-7 http://dx.doi.org/10.1002/1873-3468.12035
Fran Maathuis (University of York) is the leader on this study that assesses the transport properties of two different vacuolar-localised AtTPK1 alleles identified for a study of natural variation in Arabidopsis. They use patch-clamping the interrogate the difference between these proteins from Lansberg (Ler) and Kas-2 ecotypes, when they showed different levels of Ca(2+) dependence. This coincided with lower water loss in either the presence of absence of ABA and higher Ler AtTPK1 activity at similar cytoplasmic [Ca]. The authors present a model that helps to explain their findings.
Dumont M, Lehner A, Vauzeilles B,, Malassis J, Marchant A, Smyth K, Linclau B, Baron A, Mas Pons J, Anderson CT, Schapman D, Galas L, Mollet JC, Lerouge P (2015) Plant cell wall imaging by metabolic click-mediated labelling of rhamnogalacturonan II using azido 3-deoxy-D-manno-oct-2-ulosonic acid. Plant Journal. http://dx.doi.org/10.1111/tpj.13104
The majority of the authors on this Technical Advance are from French institutions but also includes UK plant scientist Alan Marchant (University of Southampton). They investigate the chemistry of Arabidopsis and tobacco cell walls, specifically looking at the incorperation of 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo), a monosaccharide that is only found the cell wall pectin rhamnogalacturonan-II (RG-II). They show that RG-II is found in the primary cell wall including within the root elongation zone. Finally they show that monitoring of Kdo is an effective way to study the synthesis and redistribution of RG-II during root growth.
Amos W (2015) Heterozygosity increases microsatellite mutation rate. Biol Lett. http://dx.doi.org/10.1098/rsbl.2015.0929 Open Access
This study is led by Professor William Amos who is based in the Zoology department at Cambridge. He is not usually a plant science researcher but used the excellent 1001genome project to investigate heterozygote instability (HI) in Arabidopsis. He looked at AC microsatellite sequences from over 1100 genome sequences and used rare alleles as a surrogate for more recent mutations, ultimately showing that rare alleles are more likely to occur at locus-population combinations with higher heterozygosity even when all populations carry exactly the same number of alleles. This shows that local heterozygosity causes more mutations and represents a positive feedback loop.