Migration routes and important stopover sites of endangered Oriental white storks (Ciconia boyciana), as revealed by satellite tracking

From 1998 through 2000, we tracked the autumnal migrations of 13 oriental white storks (Ciconia boyciana) by satellite in order to identify their important stopover sites. The storks were successfully tracked and provided data on partial (n= 4) or complete (n= 9) autumnal migration between the Russian Far East breeding sites and the wintering sites in southeastern China. Twenty-seven stopover sites were identified, the most important of which were in Tonghe Peat Moor (46.095°N, 128.942°E), Momoge Nature Reserve (45.945°N, 123.939°E), and Jiantuozhi Gley Mire (39.221°N, 118.672°E). The connectedness between each stopover site and its surrounding stay sites was also evaluated; the results suggested that the stopover sites situated on the seashores of Liaodong Bay, Bohai Bay, and Laizhou Bay in eastern China are less connected than the others. We concluded that, among the sites studied, Jiantuozhi Gley Mire on the northern shore of Bohai Bay should have a higher priority for protection for two reasons: it is used by many storks, in common, for relatively long periods; and it is at higher risk of being isolated from the migration route network

AA amyloidosis-resistant CE/J mice have Saa1 and Saa2 genes that encode an identical SAA isoform

The CE/J mouse strain is resistant to amyloid A protein (AA) amyloidosis. In contrast to AA amyloidosis-susceptible mouse strains that concomitantly express serum amyloid A precursor protein (SAA) types 1 and 2 isoforms encoded by the Saa1 and Saa2 genes, respectively, in response to inflammatory stimulation from the liver, CE/J mice express only a single SAA isoform named SAA2.2. In addition, CE/J mice uniquely possess a Q30L amino acid substitution in SAA2.2 that inhibits amyloidogenesis. To elucidate the genetic basis underlying the expression of only a single SAA isoform in this strain, we conducted PCR cloning and nucleotide sequencing of the Saa1 and Saa2 genes from the CE/J genome. We revealed that CE/J mice possess functional Saa1 and Saa2 genes. Intriguingly, the two genes were identical with respect to amino acid sequence, each encoding the SAA2.2 isoform. RT-PCR analysis of inflamed liver tissue from CE/J mice demonstrated that both genes are expressed at equivalent levels. Reporter assays revealed that promoter/enhancer sequences of Saa1 and Saa2 genes in CE/J are also functional. These results indicate that the SAA2.2 isoform in CE/J is a mixture of Saa1 and Saa2 gene products.ArticleAMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS. 21(1):1-8 (2014)journal articl

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西日本言語研究会第3回大

Hereditary cataract of the Nakano mouse: Involvement of a hypomorphic mutation in the coproporphyrinogen oxidase gene

The Nakano cataract (NCT) is a recessive disorder in the mouse linked to the nct locus on chromosome 16. In this study, we positionally cloned the critical gene in the nct locus. Herein, we report that cataracts in the BALB/c-nct/nct mouse are caused by a hypomorphic mutation in the coproporphyrin oxidase gene (Cpox), encoding the enzyme responsible for catalyzing oxidative decarboxylation of the heme precursor, coproporphyrinogen III, in the heme biosynthetic pathway. BALB/c-nct/nct mice are homozygous for a G to T nucleotide substitution in the Cpox gene, which results in a p.R380L amino acid substitution in the CPDX protein. The CPDX isoform with the p.R380L substitution retained only 15% of the activity of the wild type isoform. BALB/c-nct/nct mice had excessive accumulation of coproporphyrin HI in the lens. The NCT phenotype was normalized by the introduction of a wild type Cpox transgene. The mechanisms by which impairment of CPDX leads to lens opacity in the NCT are elusive. However, our data illuminate a hitherto unanticipated involvement of the heme biosynthesis pathway in lens physiology.ArticleEXPERIMENTAL EYE RESEARCH. 112:45-50 (2013)journal articl

The brightest UV-selected galaxies in protoclusters at z∼4z\sim4: Ancestors of Brightest Cluster Galaxies?

We present the results of a survey of the brightest UV-selected galaxies in protoclusters. These proto-brightest cluster galaxy (proto-BCG) candidates are drawn from 179 overdense regions of $g$-dropout galaxies at $z\sim4$ from the Hyper Suprime-Cam Subaru Strategic Program identified previously as good protocluster candidates. This study is the first to extend the systematic study of the progenitors of BCGs from $z\sim2$ to $z\sim4$. We carefully remove possible contaminants from foreground galaxies and, for each structure, we select the brightest galaxy that is at least 1 mag brighter than the fifth brightest galaxy. We select 63 proto-BCG candidates and compare their properties with those of galaxies in the field and those of other galaxies in overdense structures. The proto-BCG candidates and their surrounding galaxies have different rest-UV color $(i - z)$ distributions to field galaxies and other galaxies in protoclusters that do not host proto-BCGs. In addition, galaxies surrounding proto-BCGs are brighter than those in protoclusters without proto-BCGs. The image stacking analysis reveals that the average effective radius of proto-BCGs is $\sim28\%$ larger than that of field galaxies. The $i-z$ color differences suggest that proto-BCGs and their surrounding galaxies are dustier than other galaxies at $z\sim4$. These results suggest that specific environmental effects or assembly biasses have already emerged in some protoclusters as early as $z \sim 4$, and we suggest that proto-BCGs have different star formation histories than other galaxies in the same epoch.Comment: 18 pages, 11 figures, Accepted for publication in Ap