Guanylate-Binding Protein 1はTBK1のリン酸化を介して感染誘導性のオートファジーを制御する

京都大学新制・課程博士博士(医学)甲第24315号医博第4909号新制||医||1062(附属図書館)京都大学大学院医学研究科医学専攻(主査)教授 杉田 昌彦, 教授 椛島 健治, 教授 秋山 芳展学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDFA

Slow quench dynamics of the Kitaev model: anisotropic critical point and effect of disorder

We study the non-equilibrium slow dynamics for the Kitaev model both in the presence and the absence of disorder. For the case without disorder, we demonstrate, via an exact solution, that the model provides an example of a system with an anisotropic critical point and exhibits unusual scaling of defect density $n$ and residual energy $Q$ for a slow linear quench. We provide a general expression for the scaling of $n$ ($Q$) generated during a slow power-law dynamics, characterized by a rate $\tau^{-1}$ and exponent $\alpha$, from a gapped phase to an anisotropic quantum critical point in $d$ dimensions, for which the energy gap $\Delta_{\vec k} \sim k_i^z$ for $m$ momentum components ($i=1..m$) and $\sim k_i^{z'}$ for the rest $d-m$ components ($i=m+1..d$) with $z\le z'$: $n \sim \tau^{-[m + (d-m)z/z']\nu \alpha/(z\nu \alpha +1)}$ ($Q \sim \tau^{-[(m+z)+ (d-m)z/z']\nu \alpha/(z\nu \alpha +1)}$). These general expressions reproduce both the corresponding results for the Kitaev model as a special case for $d=z'=2$ and $m=z=\nu=1$ and the well-known scaling laws of $n$ and $Q$ for isotropic critical points for $z=z'$. We also present an exact computation of all non-zero, independent, multispin correlation functions of the Kitaev model for such a quench and discuss their spatial dependence. For the disordered Kitaev model, where the disorder is introduced via random choice of the link variables $D_n$ in the model's Fermionic representation, we find that $n \sim \tau^{-1/2}$ and $Q\sim \tau^{-1}$ ($Q\sim \tau^{-1/2}$) for a slow linear quench ending in the gapless (gapped) phase. We provide a qualitative explanation of such scaling.Comment: 10 pages, 11 Figs. v

The hrp genes of Pseudomonas cichorii are essential for pathogenicity on eggplant but not on lettuce

Pseudomonas cichorii causes necrotic lesions in eggplant and rot in lettuce. Through transposon insertion into P. cichorii strain SPC9018 we produced two mutants, 4-57 and 2-99, that lost virulence on eggplant but not lettuce. Analyses showed that a transposon was inserted into the hrpG gene in 4-57 and the hrcT gene in 2-99. Nucleotide sequences of the hrp genes of SPC9018 are homologous to those of Pseudomonas viridiflava BS group strains. The pathogenicity of 4-57 on eggplant was restored by transformation with an hrpF operon, originating from either SPC9018 or the BS group member P. viridiflava strain 9504 (Pv9504). These data suggested the involvement of hrp genes in the pathogenicity of SPC9018 on eggplant, and functional conservation of hrpF operons between SPC9018 and Pv9504. Both the hrpS mutant and the hrpL mutant were unable to cause necrotic lesions on eggplant leaves but retained their pathogenicity against lettuce. These results suggest that the pathogenicity of P. cichorii is hrp-dependent in eggplant, but not in lettuce