エンドウ PISUM SATIVUM L. ニ オケル HISTIDINE セヨウ ニ ヨル ニッケル ドクセイ ケイゲン コウカ

HistidineがNi超集積植物以外の植物におけるNi耐性に関与しているか否かについて明らかにする目的で,histidineが養液栽培のエンドウ(Pisum sativum L.)のNi耐性に与える影響を検討した。植物体内のhistidine含有率はNi施用により増加した。また,Ni施用によって減少した生育量は外因性のhistidineをNiと同時に施用すると軽減された。予めhistidineを植物体に吸収させた後にNiを施用すると,それらを同時に添加した場合よりも低かったがNi毒性軽減効果は認められた。従って,外因性のhistidineは培養液中および植物体内で,ある程度Niを無毒化していることが考えられた。Effects of histidine on nickel tolerance of pea (Pisum sativa L.) were investigated, to determine whether histidine participates in Ni tolerance in plants other than Ni hyperaccumulation plants. Histidine content in pea increased by the treatment with Ni. In addition, exogenous histidine reduced the inhibitory effects of Ni on the growth of pea. When adding nickel after histidine (and then histidine was removed from culture medium), the effect of histidine was lower than in the case in which it was added simultaneously. Therefore, it is suggested that exogenous histidine detoxifies Ni to some extent in the culture medium and in the plant

The viability of solar photovoltaics With specific reference to building integrated photovoltaics cladding systems

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Plots of the individual body weights of DW-<i>Tpst2^grt</i>, BC-<i>Tpst2^grt</i> and 129-<i>Tpst2^grt</i> mice at 8 weeks of age.

<p>Individual numbers are given in parentheses. Mean value and the standard deviation (s.d.) are indicated by horizontal and vertical lines, respectively.</p

Linkage maps displaying the QTL using the first principal component as an indicator for CH.

<p>A) Genome-wide linkage maps. B) Details of highly significant linkages on Chr 2. Suggestive, significant and highly significant values are 6.9, 13.7 and 21.8 for male, 7.0, 14.1 and 23.0 for female, respectively. The maximum LRS score on Chr 2 is 28.9 for male and 27.0 for female, respectively. Horizontal black bars in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031035#pone-0031035-g002" target="_blank">Fig. 2B</a> indicate 95% confidence intervals.</p

Characteristics of QTLs for growth retardation.

<p>The microsatellite markers linked to the indicator for CH with the highest LRS value on each Chr, percentage of the variance, genome-wide <i>P</i> value detected by marker regression analysis based on 10000 permutation replicates and body weights of each genotype at 10 weeks age are indicated. %: percentage of the variance. <i>P</i>: genome-wide <i>P</i> value as calculated by QTX software. Means ± s.d. are shown.</p><p>*: <i>P</i><0.01.</p

The severity of growth retardation in BC-<i>Tpst2^grt</i> mice is related to thyroid hypoplasia.

<p>A) Representative cross-sections of thyroid glands of BC-<i>Tpst2^grt</i> mice at 10 weeks of age. Upper: a male BC-<i>Tpst2^grt</i> mouse with severe growth retardation (body weight was 35.2% that of the littermate control; thyroid index = 16.3%). Lower: a male BC-<i>Tpst2^grt</i> mouse with mild growth retardation (body weight was 81.4% that of the littermate control; thyroid index = 47.4%). B) Plots of body weight and thyroid index of BC-<i>Tpst2^grt</i> at 10 weeks of age. Open triangles: BC-<i>Tpst2^grt</i> homozygous for <i>D2Mit255</i> (n = 8 and 6 for male and female, respectively), solid triangles: BC-<i>Tpst2^grt</i> heterozygous for <i>D2Mit255</i> (n = 6 and 6 for male and female, respectively), blue triangles: the average of DW-<i>Tpst2^grt</i> (n = 4 and 3 for male and female, respectively), red triangles: the average of 129-<i>Tpst2^grt</i> (n = 3 and 4 for male and female, respectively). C) Comparison of thyroid indices between genotypes at <i>D2Mit255</i> in BC-<i>Tpst2^grt</i> mice. a: homozygous, b: heterozygous for <i>D2Mit255</i>, respectively. Individual numbers are given in parentheses. Vertical lines indicate s.d. N.S.: not significant.</p

Evaluation of the effect of <i>Lrch</i> on TD-associated growth retardation by congenic strain analysis.

<p>A) Schematic diagram of the genomic structure surrounding <i>Lrch</i> in CG mice. Gray bars indicate the minimum genomic regions derived from DW. A black bar indicates a genomic region into which 129-derived alleles were introduced. Dotted bars represent recombined regions between the DW and 129 genomes. The numbers to the left of the bars represent physical locations based on the MGI. B) Growth curves of CG mice. a: littermate controls, b: CG-<i>Tpst2^grt</i> mice heterozygous for the 129-derived <i>Lrch</i> allele, c: CG-<i>Tpst2^grt</i> mice without the 129-derived <i>Lrch</i> allele. Individual numbers of a, b, c are 5, 4 and 5 for males, and 9, 5 and 2 for females, respectively. Vertical lines indicate s.d. <i>P</i><0.05: *; b versus c, †; b versus a, ‡; c versus a. C) Thyroid indices of CG-<i>Tpst2^grt</i>. Individual numbers are given in parentheses.</p

Identification of genetic loci affecting the establishment and development of Echinococcus multilocularis larvae in mice

Alveolar echinococcosis (AE) is a severe hepatic disorder caused by larval infection by the fox tapeworm Echinococcus multilocularis. The course of parasitic development and host reactions are known to vary significantly among host species, and even among different inbred strains of mice. As reported previously, after oral administration of parasite eggs, DBA/2 (D2) mice showed a higher rate of cyst establishment and more advanced protoscolex development in the liver than C57BL/6 (B6) mice. These findings strongly suggest that the outcome of AE is affected by host genetic factor(s). In the present study, the genetic basis of such strain-specific differences in susceptibility/resistance to AE in murine models was studied by whole-genome scanning for quantitative trait loci (QTLs) using a backcross of (B6 × D2)F1 and D2 mice with varying susceptibility to E. multilocularis infection. For cyst establishment, genome linkage analysis identified one suggestive and one significant QTL on chromosomes (Chrs.) 9 and 6, respectively, whereas for protoscolex development, two suggestive and one highly significant QTLs were detected on Chrs. 6, 17 and 1, respectively. Our QTL analyses using murine AE models revealed that multiple genetic factors regulated host susceptibility/resistance to E. multilocularis infection. Moreover, our findings show that establishment of the parasite cysts in the liver is affected by QTLs that are distinct from those associated with the subsequent protoscolex development of the parasite, indicating that different host factors are involved in the host–parasite interplay at each developmental stage of the larval parasite. Further identification of responsible genes located on the identified QTLs could lead to the development of effective disease prevention and control strategies, including an intensive screening and clinical follow-up of genetically high-risk groups for AE infection