Genetic Variation and Phylogeny of Wabisuke Camellias by Amplified Fragment Length Polymorphism (AFLP) Analysis

Amplified fragment length polymorphism (AFLP) analysis was conducted on the wabisuke camellia and its relative camellia species. Genetic polymorphism was identified among the ‘Uraku’ camellia, its offspring ‘Tosa-uraku’ and Camellia japonica, whereas the two accessions of the old ‘Uraku’ showed monomorphism in all the fragments. The results suggested that the two old ‘Uraku’ trees are asexually-propagated clonal strains. The genetic distance between wabisuke cultivars and Chinese camellias and between wabisuke camellias and C. sinensis was much further than that between wabisuke cultivars and Camellia japonica. It has also been suggested that wabisuke camellias can be classified into two subgroups, I-1 and I-2, and that Subgroup I-2 originated from C. japonica, while Subgroup I-1, including ‘Uraku’ (synonym: ‘Tarokaja’), was developed by the repeated hybridization of C. japonica to interspecific hybrids with the Chinese camellias, e.g., C. pitardii var. pitardii, or by the involvement of related species not investigated in this study

Inheritance of Bulb Dormancy and Early Flowering Ability in F_1 Progenies of Intra– and Interspecific Crosses of Lilium formosanum and L. longiflorum

One–year–old seedlings of the northern populations of Lilium longiflorum in the Ryukyu Archipelago have deep dormancy in summer, whereas those of the southern populations of L. longiflorum and L. formosanum show lack or reduction of dormancy. Dormancy status of the F_1 progenies of intraspecific hybrids among L. longiflorum with different degrees of dormancy and interspecific hybrids between L. formosanum and L. longiflorum was studied in an open field condition. Three populations of L. longiflorum, Yakushima (LYA) and Kikai Jima (LKI) in the Ryukyu Archipelago, Japan and Pitouchiao (LPI), Taiwan and two populations of L. formosanum, Wulai (FWU), Taiwan and Fukuoka (FFU), Japan were used. FFU, FWU, LPI and hybrids of FFU × FWU, FFU × LPI and FWU × LPI continued developing leaves in summer and flowered in a year after seed sowing, while LYA and LKI and the hybrids with them did not. Since FFU, FWU and LPI are categorized as non–dormant populations and LKI and LYA as deep dormant, the bulb dormancy seems to be dominant, while early flowering ability is recessive in the F_1 progenies

Enterohepatic Transcription Factor CREB3L3 Protects Atherosclerosis via SREBP Competitive Inhibition

動脈硬化発症を制御する転写因子の相互作用を発見. 京都大学プレスリリース. 2020-12-09.Background and Aims: cAMP responsive element-binding protein 3 like 3 (CREB3L3) is a membrane-bound transcription factor involved in the maintenance of lipid metabolism in the liver and small intestine. CREB3L3 controls hepatic triglyceride and glucose metabolism by activating plasma fibroblast growth factor 21 (FGF21) and lipoprotein lipase. In this study, we intended to clarify its effect on atherosclerosis. Methods: CREB3L3-deficifient, liver-specific CREB3L3 knockout, intestine-specific CREB3L3 knockout, both liver- and intestine-specific CREB3L3 knockout, and liver CREB3L3 transgenic mice were crossed with LDLR−/− mice. These mice were fed with a Western diet to develop atherosclerosis. Results: CREB3L3 ablation in LDLR−/− mice exacerbated hyperlipidemia with accumulation of remnant APOB-containing lipoprotein. This led to the development of enhanced aortic atheroma formation, the extent of which was additive between liver- and intestine-specific deletion. Conversely, hepatic nuclear CREB3L3 overexpression markedly suppressed atherosclerosis with amelioration of hyperlipidemia. CREB3L3 directly upregulates anti-atherogenic FGF21 and APOA4. In contrast, it antagonizes hepatic sterol regulatory element-binding protein (SREBP)-mediated lipogenic and cholesterogenic genes, and regulates intestinal liver X receptor-regulated genes involved in the transport of cholesterol. CREB3L3 deficiency results in the accumulation of nuclear SREBP proteins. Because both transcriptional factors share the cleavage system for nuclear transactivation, full-length CREB3L3 and SREBPs in the endoplasmic reticulum (ER) functionally inhibit each other. CREB3L3 promotes the formation of the SREBP-insulin induced gene 1 (SREBP-INSIG1) complex to suppress SREBPs for ER-Golgi transport, resulting in ER retention and inhibition of proteolytic activation at the Golgi, and vice versa. Conclusions: CREB3L3 has multi-potent protective effects against atherosclerosis owing to new mechanistic interaction between CREB3L3 and SREBPs under atherogenic conditions