As a base for human transcriptome and functional genomics, we created the "full-length long Japan" (FLJ) collection of sequenced human cDNAs. We determined the entire sequence of 21,243 selected clones and found that 14,490 cDNAs (10,897 clusters) were unique to the FLJ collection. About half of them (5,416) seemed to be protein-coding. Of those, 1,999 clusters had not been predicted by computational methods. The distribution of GC content of nonpredicted cDNAs had a peak at ∼58% compared with a peak at ∼42%for predicted cDNAs. Thus, there seems to be a slight bias against GC-rich transcripts in current gene prediction procedures. The rest of the cDNAs unique to the FLJ collection (5,481) contained no obvious open reading frames (ORFs) and thus are candidate noncoding RNAs. About one-fourth of them (1,378) showed a clear pattern of splicing. The distribution of GC content of noncoding cDNAs was narrow and had a peak at ∼42%, relatively low compared with that of protein-coding cDNAs.

While performing a nationwide survey of hepatitis E virus (HEV) infection among 450 wild boars (Sus scrofa leucomystax) that had been captured in Japan between November 2005 and March 2010, we found 16 boars (3.6 %) with ongoing HEV infection: 11 had genotype 3 HEV, four had genotype 4 HEV and the remaining boar was infected with HEV of an unrecognized genotype (designated wbJOY_06). The entire wbJOY_06 genome was sequenced and was found to comprise 7246 nt excluding the poly(A) tail. The wbJOY_06 isolate was highly divergent from known genotype 1-4 HEV isolates derived from humans, swine, wild boars, deer, mongoose and rabbits (n5145) by 22.6-27.7 %, rat HEV isolates (n52) by 46.0-46.2 %, and avian HEV isolates (n55) by 52.5-53.1 % over the entire genome. A Simplot analysis revealed no significant recombination between the existing HEV strains of genotypes 1-4. Therefore, we propose that the wbJOY_06 isolate is the first member of a previously unidentified genotype.The hepatitis E virus (HEV) was first identified as a leading cause of acute and fulminant hepatitis linked to faecal-oral transmission in tropical and subtropical countries. However, hepatitis E has been found to be endemic in industrialized countries, including Japan, the USA and European countries, where autochthonous HEV infections are an emerging concern (Dalton et al., 2008;Okamoto et al., 2003;Purcell & Emerson, 2008). It has recently been reported that zoonotic food-borne transmission of HEV from domestic pigs, wild boars and wild deer to humans plays an important role in the occurrence of cryptic hepatitis E in industrialized countries, including Japan and France, where people have distinctive habits of eating uncooked or undercooked meat (including the liver and colon/intestine of animals) (Colson et al., 2010;Matsuda et al., 2003; Tamada et al., 2004;Tei et al., 2003;Yazaki et al., 2003).HEV is a non-enveloped virus and its genome is a positivesense ssRNA, which is capped and polyadenylated (Kabrane-Lazizi et al., 1999;Tam et al., 1991). It is classified as the sole member of the genus Hepevirus in the family Hepeviridae . The genome is approximately 7.2 kb in size and contains three ORFs that encode non-structural proteins involved in replication (ORF1), a capsid protein consisting of 660 aa (ORF2), and a small protein of only 113-114 aa (ORF3) that is essential for viral infectivity in animals (Graff et al., 2005;Huang et al., 2007) and virion egress (Emerson et al., 2010;Yamada et al., 2009a). Four genotypes of HEV that infect humans have been identified Lu et al., 2006;Okamoto, 2007). HEV genotypes 1 and 2 are restricted to humans and associated with outbreaks of hepatitis E as water-borne epidemics in developing countries, whereas HEV genotypes 3 and 4 are zoonotic and responsible for sporadic cases of hepatitis E worldwide.Recently, significant progress has been made in understanding the animal reservoirs of HEV (Meng, 2010;Pavio et al., 2010). The discoveries of animal strains of HEV from domestic pigs (Meng et al., 1997) The GenBan...

This article deals with the conjugate gradient method on a Riemannian manifold with interest in global convergence analysis. The existing conjugate gradient algorithms on a manifold endowed with a vector transport need the assumption that the vector transport does not increase the norm of tangent vectors, in order to confirm that generated sequences have a global convergence property. In this article, the notion of a scaled vector transport is introduced to improve the algorithm so that the generated sequences may have a global convergence property under a relaxed assumption. In the proposed algorithm, the transported vector is rescaled in case its norm has increased during the transport. The global convergence is theoretically proved and numerically observed with examples. In fact, numerical experiments show that there exist minimization problems for which the existing algorithm generates divergent sequences, but the proposed algorithm generates convergent sequences.Comment: 22 pages, 8 figure

In this paper, we characterized the Wx-mq gene for low amylose content in a rice variety, Milky Queen, at the molecular level. The Wx-mq gene was cloned by RT-PCR, and a nearly full-length cDNA sequence of the gene was determined. Sequence comparison between the Wx-mq gene and the wild type allele (Wx-b), cloned from cv. Koshihikari, revealed that two base changes existed within the coding region; a G to A base change at nucleotide position 497 and a T to C base change at nucleotide position 595. Each nucleotide substitution should generate a missense base change (an Arg-158 to His-158 change in exon4, and a Tyr-191 to His-191 change in exon5). However, it is not known which missense mutation is essential for the activity of the WX protein. To identify rice varieties and lines, which harbored the Wx-mq gene, PCR primers were designed at the gene level. These primers were able to amplify the Wx-mq specific 741 bp band in Milky Queen, and in other rice variety and lines, Milky Princess, Joiku 436 and Etsunan 190, all of which have the same pedigree as that of Milky Queen. On the other hand, no 741 bp band was amplified with the primers in Koshihikari which harbored the wild type allele (Wx-b), and the other low-amylose content variety and line, Snow Pearl and NM391, which do not have the pedigree. Thus, it is possible to detect the Wx-mq gene by PCR.

To identify the chromosomal regions controlling the eating quality of cooked rice, we performed a quantitative trait locus (QTL) analysis using 93 backcross inbred lines (BILs) and 39 chromosome segment substitution lines (CSSLs) derived from crosses between a japonica rice cultivar Koshihikari (glossier appearance, tasty, sticky and soft eating quality of rice when cooked) and an indica cultivar Kasalath (less glossy appearance, less sticky and hard eating quality of rice when cooked). We evaluated the eating quality of rice including overall evaluation (OE), glossiness (GL), taste (TA), stickiness (ST) and hardness (HA) in each line based on the sensory test of cooked rice. Twenty-one QTLs for eating quality were mapped to eight regions on chromosomes 1, 2, 3 (two regions), 6, 7, 9 and 10. The Koshihikari alleles at 19 out of 21 QTLs increased the eating quality, while the Kasalath alleles at the other two QTLs increased the eating quality. We also mapped the QTLs for chemical properties, such as amylose content (AC) and protein content (PC), which affected the eating quality. Four QTLs in the terminal region of the short arm of chromosome 3 and five QTLs on chromosome 6 for eating quality were mapped to the same region as that of the QTLs for AC. Three QTLs on chromosome 1 for eating quality were also mapped to the same region as that of a QTL for PC. The chromosome positions of the other QTLs for eating quality did not coincide with those of the QTLs for AC and PC. Six out of 21 QTLs for eating quality, qTA3, qOE6, qGL6, qTA6, qST6 and qHA6, were commonly identified by analysis using both BILs and CSSLs. One QTL, qTA3, was not a locus of AC, PC or known eating genes. Thus the QTL was mapped in the interval between the SSR markers RM1332 and RM6676 in the middle region of the short arm of chromosome 3 by fine mapping of three sub-CSSLs. Five QTLs, qOE6, qGL6, qTA6, qST6 and qHA6, seemed to be associated with the Waxy (Wx) gene located on chromosome 6.