| 1. |
- Benson, Samuel L, et al.
(författare)
-
An intact light harvesting complex I antenna system is required for complete state transitions in Arabidopsis
- 2015
-
Ingår i: Nature plants. - : Nature Publishing Group. - 2055-026X. ; 1:12
-
Tidskriftsartikel (refereegranskat)abstract
- Efficient photosynthesis depends on maintaining balance between the rate of light-driven electron transport occurring in photosystem I (PSI) and photosystem II (PSII), located in the chloroplast thylakoid membranes. Balance is achieved through a process of 'state transitions' that increases energy transfer towards PSI when PSII is overexcited (state II), and towards PSII when PSI is overexcited (state I). This is achieved through redox control of the phosphorylation state of light-harvesting antenna complex II (LHCII). PSI is served by both LHCII and four light-harvesting antenna complex I (LHCI) subunits, Lhca1, 2, 3 and 4. Here we demonstrate that despite unchanged levels of LHCII phosphorylation, absence of specific Lhca subunits reduces state transitions in Arabidopsis. The severest phenotype-observed in a mutant lacking Lhca4 (Delta Lhca4)-displayed a 69% reduction compared with the wild type. Yet, surprisingly, the amounts of the PSI-LHCI-LHCII supercomplex isolated by blue native polyacrylamide gel electrophoresis (BN-PAGE) from digitonin-solubilized thylakoids were similar in the wild type and Delta Lhca mutants. Fluorescence excitation spectroscopy revealed that in the wild type this PSI-LHCI-LHCII supercomplex is supplemented by energy transfer from additional LHCII trimers in state II, whose binding is sensitive to digitonin, and which are absent in Delta Lhca4. The grana margins of the thylakoid membrane were found to be the primary site of interaction between this 'extra' LHCII and the PSI-LHCI-LHCII supercomplex in state II. The results suggest that the LHCI complexes mediate energetic interactions between LHCII and PSI in the intact membrane.
|
|
| 2. |
- Sandholm, Niina, et al.
(författare)
-
The genetic landscape of renal complications in type 1 diabetes
- 2017
-
Ingår i: Journal of the American Society of Nephrology. - 1046-6673. ; 28:2, s. 557-574
-
Tidskriftsartikel (refereegranskat)abstract
- Diabetes is the leading cause of ESRD. Despite evidence for a substantial heritability of diabetic kidney disease, efforts to identify genetic susceptibility variants have had limited success. We extended previous efforts in three dimensions, examining a more comprehensive set of genetic variants in larger numbers of subjects with type 1 diabetes characterized for a wider range of cross-sectional diabetic kidney disease phenotypes. In 2843 subjects, we estimated that the heritability of diabetic kidney disease was 35% (P=6.4310-3). Genome-wide association analysis and replication in 12,540 individuals identified no single variants reaching stringent levels of significance and, despite excellent power, provided little independent confirmation of previously published associatedvariants.Whole-exome sequencing in 997 subjects failed to identify any large-effect coding alleles of lower frequency influencing the risk of diabetic kidney disease. However, sets of alleles increasing body mass index (P=2.2310-5) and the risk of type 2 diabetes (P=6.1310-4) associated with the risk of diabetic kidney disease.Wealso found genome-wide genetic correlation between diabetic kidney disease and failure at smoking cessation (P=1.1310-4). Pathway analysis implicated ascorbate and aldarate metabolism (P=9.0310-6), and pentose and glucuronate interconversions (P=3.0310-6) in pathogenesis of diabetic kidney disease. These data provide further evidence for the role of genetic factors influencing diabetic kidney disease in those with type 1 diabetes and highlight some key pathways that may be responsible. Altogether these results reveal important biology behind the major cause of kidney disease.
|
|
