Effect of temperature on achene germination in five Mutisieae understory herbaceous species（Asteraceae）

We measured the final germination rates of achenes, the number of days needed to accomplish 50% of the final germination（T50）, and mortalities under various temperatures in the range 5 to 25℃for five understory peren-nial herbs（four species with large achenes of ca. 10 mg weight : Pertya robusta, P . triloba, P . rigidula and Ain-sliaea acerifolia var. subapoda, and one species with small achenes（1mg）: A. apiculata）to investigate variation of these traits. Achenes were collected in Ogawa and Mito in Ibaraki Prefecture, and in Iwakuni in Fukui Prefec-ture. T50 ranged from 35 to 76 days at 5℃and became shorter with increasing temperature. The final germina-tion rates of most samples were over 95%. Ainsliaea acerifolia had the longest T50（76 days）and the lowest final germination rate（86.1%）at 5℃, showing a dormant ability to some extent. Moreover, A. apiculata possessing small achenes showed a lower final germination rate（83%）at 25℃, and dormancy at higher temperatures. Fun-gal attack was thought to cause the death of achenes during the germination period, and mortalities increased with increasing temperature. However, there were no significant differences in final germination rates and T50s between two populations of P . robusta from Ogawa and Mito, though the Ogawa population had a higher mor-tality than the Mito population（27% vs. 18% at 25℃）. Mortalities were higher in P . triloba and P . rigidula than in the other species. There were intra- and interspecific variations of temperature dependency of achene mortal-ity during germination, and these variations may be one of the factors limiting the distribution of each species

人工被陰下での光合成特性と実生の生存からみたハルジオンの耐陰性

[論文

UCP1発現調節化合物のスクリーニングと評価のためのUcp1レポーターシステムの樹立に関する研究

京都大学新制・課程博士博士(農学)甲第24110号農博第2515号新制||農||1093(附属図書館)学位論文||R4||N5401(農学部図書室)京都大学大学院農学研究科食品生物科学専攻(主査)教授 井上 和生, 教授 谷 史人, 准教授 後藤 剛学位規則第4条第1項該当Doctor of Agricultural ScienceKyoto UniversityDGA

β-adrenergic Receptor Stimulation Revealed a Novel Regulatory Pathway via Suppressing Histone Deacetylase 3 to Induce Uncoupling Protein 1 Expression in Mice Beige Adipocyte

Browning of adipose tissue has been prescribed as a potential way to treat obesity, marked by the upregulation of uncoupling protein 1 (Ucp1). Several reports have suggested that histone deacetylase (HDAC) might regulate Ucp1 by remodelling chromatin structure, although the mechanism remains unclear. Herein, we investigate the effect of β-adrenergic receptor (β-AR) activation on the chromatin state of beige adipocyte. β-AR-stimulated Ucp1 expression via cold (in vivo) and isoproterenol (in vitro) resulted in acetylation of histone activation mark H3K27. H3K27 acetylation was also seen within Ucp1 promoter upon isoproterenol addition, favouring open chromatin for Ucp1 transcriptional activation. This result was found to be associated with the downregulation of class I HDAC mRNA, particularly Hdac3 and Hdac8. Further investigation showed that although HDAC8 activity decreased, Ucp1 expression was not altered when HDAC8 was activated or inhibited. In contrast, HDAC3 mRNA and protein levels were simultaneously downregulated upon isoproterenol addition, resulting in reduced recruitment of HDAC3 to the Ucp1 enhancer region, causing an increased H3K27 acetylation for Ucp1 upregulation. The importance of HDAC3 inhibition was confirmed through the enhanced Ucp1 expression when the cells were treated with HDAC3 inhibitor. This study highlights the novel mechanism of HDAC3-regulated Ucp1 expression during β-AR stimulation

The Mevalonate Pathway Is Indispensable for Adipocyte Survival

Summary: The mevalonate pathway is essential for the synthesis of isoprenoids and cholesterol. Adipose tissue is known as a major site for cholesterol storage; however, the role of the local mevalonate pathway and its synthesized isoprenoids remains unclear. In this study, adipose-specific mevalonate pathway-disrupted (aKO) mice were generated through knockout of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase (HMGCR). aKO mice showed serious lipodystrophy accompanied with glucose and lipid metabolic disorders and hepatomegaly. These metabolic variations in aKO mice were dramatically reversed after fat transplantation. In addition, HMGCR-disrupted adipocytes exhibited loss of lipid accumulation and an increase of cell death, which were ameliorated by the supplementation of mevalonate and geranylgeranyl pyrophosphate but not farnesyl pyrophosphate and squalene. Finally, we found that apoptosis may be involved in adipocyte death induced by HMGCR down-regulation. Our findings indicate that the mevalonate pathway is essential for adipocytes and further suggest that this pathway is an important regulator of adipocyte turnover. : Pathophysiology; Molecular Mechanism of Behavior; Diabetology; Specialized Functions of Cells Subject Areas: Pathophysiology, Molecular Mechanism of Behavior, Diabetology, Specialized Functions of Cell

Mevalonate biosynthesis pathway regulates the development and survival of brown adipocytes

Summary: The high thermogenic activity of brown adipose tissue (BAT) has received considerable attention. Here, we demonstrated the role of the mevalonate (MVA) biosynthesis pathway in the regulation of brown adipocyte development and survival. The inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the rate-limiting enzyme in the MVA pathway and the molecular target of statins, suppressed brown adipocyte differentiation by suppressing protein geranylgeranylation-mediated mitotic clonal expansion. The development of BAT in neonatal mice exposed to statins during the fetal period was severely impaired. Moreover, statin-induced geranylgeranyl pyrophosphate (GGPP) deficiency led to the apoptosis of mature brown adipocytes. Brown adipocyte-specific Hmgcr knockout induced BAT atrophy and disrupted thermogenesis. Importantly, both genetic and pharmacological inhibition of HMGCR in adult mice induced morphological changes in BAT accompanied by an increase in apoptosis, and statin-treated diabetic mice showed worsened hyperglycemia. These findings revealed that MVA pathway-generated GGPP is indispensable for BAT development and survival