52 research outputs found
Prey preference in a kleptoplastic dinoflagellate is linked to photosynthetic performance
Get PDFDinoflagellates of the family Kryptoperidiniaceae, known as “dinotoms”, possess diatom-derived endosymbionts and contain individuals at three successive evolutionary stages: a transiently maintained kleptoplastic stage; a stage containing multiple permanently maintained diatom endosymbionts; and a further permanent stage containing a single diatom endosymbiont. Kleptoplastic dinotoms were discovered only recently, in Durinskia capensis; until now it has not been investigated kleptoplastic behavior and the metabolic and genetic integration of host and prey. Here, we show D. capensis is able to use various diatom species as kleptoplastids and exhibits different photosynthetic capacities depending on the diatom species. This is in contrast with the prey diatoms in their free-living stage, as there are no differences in their photosynthetic capacities. Complete photosynthesis including both the light reactions and the Calvin cycle remain active only when D. capensis feeds on its habitual associate, the “essential” diatom Nitzschia captiva. The organelles of another edible diatom, N. inconspicua, are preserved intact after ingestion by D. capensis and expresses the psbC gene of the photosynthetic light reaction, while RuBisCO gene expression is lost. Our results indicate that edible but non-essential, “supplemental” diatoms are used by D. capensis for producing ATP and NADPH, but not for carbon fixation. D. capensis has established a species-specifically designed metabolic system allowing carbon fixation to be performed only by its essential diatoms. The ability of D. capensis to ingest supplemental diatoms as kleptoplastids may be a flexible ecological strategy, to use these diatoms as “emergency supplies” while no essential diatoms are available.Open Access funding enabled and organized by Projekt DEAL.We are grateful to Dr Benjamin Bailleul for discussing the photoactivity possibility of N. inconspicua, and to Prof Dieter Spiteller and Dr Adrien Lapointe for suggesting the feeding experiment of D. capensis with four selected diatoms. We also thank Dr Martin Stöckl, from the Bioimaging Centre at University of Konstanz, for technical support of the CLSM. Our thanks also go to Ms Selina Pucher and Mr Alexander H. Fürst for discussing the RT-qPCR data analyses and evaluation, and to Mr Niccolo Mosesso for discussing the TEM protocol improvement. This research was supported by the Bridging Stipend of University of Konstanz (No.638/20, granted to NY), the DFG Research Grant (No. YA 577/2-1, granted to NY), and the Symbiosis Model Systems Award (No. GBMF9360, granted to NY, RT, DGM, PGK) of the Gordon and Betty Moore Foundation. The CERCA Programme of Generalitat of Catalonia is also acknowledged. The Royal Botanic Garden Edinburgh is supported by the Scottish Government’s Rural and Environment Science and Analytical Services Division.info:eu-repo/semantics/publishedVersio
Detection of the quantitative trait loci for α-amylase activity on a high-density genetic map of rye and comparison of their localization to loci controlling preharvest sprouting and earliness
Full text linkNOX1 loss-of-function genetic variants in patients with inflammatory bowel disease.
Get PDFGenetic defects that affect intestinal epithelial barrier function can present with very early-onset inflammatory bowel disease (VEOIBD). Using whole-genome sequencing, a novel hemizygous defect in NOX1 encoding NAPDH oxidase 1 was identified in a patient with ulcerative colitis-like VEOIBD. Exome screening of 1,878 pediatric patients identified further seven male inflammatory bowel disease (IBD) patients with rare NOX1 mutations. Loss-of-function was validated in p.N122H and p.T497A, and to a lesser degree in p.Y470H, p.R287Q, p.I67M, p.Q293R as well as the previously described p.P330S, and the common NOX1 SNP p.D360N (rs34688635) variant. The missense mutation p.N122H abrogated reactive oxygen species (ROS) production in cell lines, ex vivo colonic explants, and patient-derived colonic organoid cultures. Within colonic crypts, NOX1 constitutively generates a high level of ROS in the crypt lumen. Analysis of 9,513 controls and 11,140 IBD patients of non-Jewish European ancestry did not reveal an association between p.D360N and IBD. Our data suggest that loss-of-function variants in NOX1 do not cause a Mendelian disorder of high penetrance but are a context-specific modifier. Our results implicate that variants in NOX1 change brush border ROS within colonic crypts at the interface between the epithelium and luminal microbes
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