Abbreviations: 3-MA, 3-methyladenine; ATG, autophagy-related; CCCP, carbonyl cyanide m-chlorophenyl hydrazone; ER, endoplasmic reticulum; FUNDC1, FUN14 Domain Containing 1; LC3, microtubule-associated protein 1 light chain 3; MAPK, mitogen-activated protein kinase; MEF, mouse embryonic fibroblast; MEK, MAPK-ERK kinase; MKK, MAP kinase kinase; PE, phosphatidylethanolamine; PINK1, PTEN-induced putative kinase protein 1; PTEN, phosphatase and tensin homolog; siRNA, short interfering RNA; SQSTM1, sequestosome 1; Tet, tetracycline.In cultured cells, not many mitochondria are degraded by mitophagy induced by physiological cellular stress. We observed mitophagy in HeLa cells using a method that relies on the pH-sensitive fluorescent protein Keima. With this approach, we found that mitophagy was barely induced by carbonyl cyanide m-chlorophenyl hydrazone treatment, which is widely used as an inducer of PARK2/Parkin-related mitophagy, whereas a small but modest amount of mitochondria were degraded by mitophagy under conditions of starvation or hypoxia. Mitophagy induced by starvation or hypoxia was marginally suppressed by knockdown of ATG7 and ATG12, or MAP1LC3B, which are essential for conventional macroautophagy. In addition, mitophagy was efficiently induced in Atg5 knockout mouse embryonic fibroblasts. However, knockdown of RAB9A and RAB9B, which are essential for alternative autophagy, but not conventional macroautophagy, severely suppressed mitophagy. Finally, we found that the MAPKs MAPK1/ERK2 and MAPK14/p38 were required for mitophagy. Based on these findings, we conclude that mitophagy in mammalian cells predominantly occurs through an alternative autophagy pathway, requiring the MAPK1 and MAPK14 signaling pathways.

Mitophagy is a process that selectively degrades mitochondria. When mitophagy is induced in yeast, the mitochondrial outer membrane protein Atg32 is phosphorylated, interacts with the adaptor protein Atg11 and is recruited into the vacuole with mitochondria. We screened kinase-deleted yeast strains and found that CK2 is essential for Atg32 phosphorylation, Atg32-Atg11 interaction and mitophagy. Inhibition of CK2 specifically blocks mitophagy, but not macroautophagy, pexophagy or the Cvt pathway. In vitro, CK2 phosphorylates Atg32 at serine 114 and serine 119. We conclude that CK2 regulates mitophagy by directly phosphorylating Atg32.

Time-resolved resonant light scattering in a disordered system is theoretically investigated. It is found that pulse excitation enables one to observe directly the relaxation of elementary excitations which is caused by disorder. In the case of weak disorder, the rapid scatteringlike and slow luminescencelike components distinctively appear. In the case of strong disorder, a continuous change from scattering to luminescence appears, which reflects the dephasing dynamics in the excited states of a disordered system. During the last decade or so there has been an increasing interest in the relationship between scattering and luminescence when the incident light frequency approaches the transition frequency in gases or in solids; luminescence is the two-step real process in which the emission of secondary radiation is independent of light absorption, while scattering is the virtual process in which the absorption and emission processes are quantum-mechanically correlated with each other. Recently, transient resonant light scattering (TRLS) by an ultrashort optical pulse has received particular attention, since it enables us to distinguish more distinctly the scattering and the luminescence, and provides us with more direct information on the fast relaxation phenomena associated with the optically excited nonequilibrium states in condensed matter. 1 " 4 The extremely fast relaxation mechanism in condensed matter has, however, been limited mainly to the vibrational degrees of freedom in regular crystals. On the other hand, disordered systems, such as mixed crystals or amorphous materials, have attracted increasing attention because of the characteristic features inherent in their random nature, such as Anderson localization, 5,6 the glass transition, 7 ' 8 fractal geometry, 9, 10 and so on. It should, however, be remarked that most of the earlier studies for disordered systems have been associated with stationary phenomena in equilibrium or near-equilibrium states.In this Letter, I first present a theoretical study of TRLS in disordered systems, which provides us with information on the dynamical relaxation phenomena for elementary excitations in disordered systems associated with the random nature of matter. I consider, as an example, electronic systems in substitutional^ disordered mixed crystals with finite band gaps.In the following theoretical analysis, we will use the coherent-potential approximation (CPA) 11 " 13 which enables us to calculate the density of states, the absorption spectrum, and the transport coefficient for a wide range of parameters. In the case of TRLS, however, the finiteness of the lifetime of excited states plays the important role, so that we have to evaluate the self-energy and the t matrix for a complex energy whose imaginary part is associated with the inverse of the lifetime. Furthermore, the vertex correction should be taken into account, since TRLS is a secondorder optical process. It should be noted that in the light-scattering phenomena, unlike the case of electrical conductivity,...

We present a general formulation to suppress pure dephasing by multipulse control. The formula is free from a specific form of interaction and is expressed in terms of the correlation function of arbitrary system-reservoir interaction. We first apply the formula to a phenomenological twolevel model where the correlation function of the interaction decays exponentially. In this case, we analytically show that the pure dephasing time is effectively lengthened by the multipulse control. Secondly, we apply the formula to the spin-boson model where a spin nonlinearly interacts with a boson reservoir. We find the multipulse control works well when the pulse interval is sufficiently shorter than the correlation time of system-reservoir interaction. Moreover, in this case, the pure dephasing can also be suppressed by adjusting the pulse interval to the period of dynamical motion of reservoir.

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We theoretically discover purely electronic polarization modes in THz frequency region in dimer Mott insulators κ-(BEDT-TTF)2X. The unusual low-frequency modes arise from the coupling between the oscillation of intradimer electric dipole moments and that of alternating interdimer bond orders. These collective motions play an important role in the dynamical dielectric properties of the dimer Mott insulators. Near the phase boundary of the dimer Mott transition, the ferroelectric ground state is realized by introducing electron-lattice coupling.PACS numbers: 71.30.+h, 78.30.Jw Low-dimensional strongly correlated electron systems with a quarter-filled band have recently attracted much attention. BEDT-TTF salts are typical two-dimensional systems with anisotropic triangular lattices, and the strong correlation and frustration act cooperatively to generate exotic phases. Among the BEDT-TTF salts, κ-(BEDT-TTF) 2 X (X: a counter anion) exhibit the Mott insulator phase [1][2][3][4][5], exotic superconducting phase [6], spin liquid phase [7][8][9], and so on. The BEDT-TTF molecular lattice is distorted to form dimers in κ-(BEDT-TTF) 2 X. Hybridized two sites can be effectively treated as a single site, and the valence band is regarded as a half-filled one. As a result, κ-(BEDT-TTF) 2 X exhibits the Mott insulator phase if the effective on-site Coulomb energy is large enough. The state is called the dimer Mott insulator.Recently quite interesting charge excitation phenomena have been observed in the dimer Mott insulators: photoinduced phase transition to a metallic state [10], and anomaly in dielectric properties [11]. In particular, the latter suggests that low-energy charge excitation exists in the dimer Mott insulators in contrast to the case of the Mott insulators.In this letter, we show for the first time that the dimer Mott insulator has THz electric polarization, which purely arises from the electron dynamics. The ferroelectricity which arises from the electron dynamics has been observed in some materials, and these ferroelectrics have unconventional origins such as charge order generation [12][13][14][15][16]. We propose another new origin of ferroelectricity in this paper.We adopt the 1/4-filled extended Hubbard Hamiltonian for holes on the two-dimensional anisotropic triangular lattice, which includes the degrees of freedom in a dimer. It is given by H = (β n,mpn,m + V n,m n n n m ) + U n n n,↑ n n,↓ , (1) where < n, m > denotes the neighbor site pairs, c n,σ (c † n,σ ) is the annihilation (creation) operator for a hole of spin σ at the site n, β n,m (V n,m ) is the transfer integral (the Coulomb interaction energy) between the sites n and m,p n,m = σ (c † m,σ c n,σ + c † n,σ c m,σ ), U is the on-site Coulomb interaction energy, n n,σ = c † n,σ c n,σ , and n n = σ n n,σ . The 4 × 4 cluster of the system size N = 16 with the periodic boundary condition is used.We calculate the quantum state excited by light pulse expressed by the vector potential A(t) = eA exp(−(t/D)2 ) cos(ω p t) of a Gaussian profile....

When mitophagy is induced in Saccharomyces cerevisiae, the mitochondrial outer membrane protein ScAtg32 interacts with the cytosolic adaptor protein ScAtg11. ScAtg11 then delivers the mitochondria to the pre-autophagosomal structure for autophagic degradation. Despite the importance of ScAtg32 for mitophagy, the expression and functional regulation of ScAtg32 are poorly understood. In this study, we identified and characterized the ScAtg32 homolog in Pichia pastoris (PpAtg32). Interestingly, we found that PpAtg32 was barely expressed before induction of mitophagy and was rapidly expressed after induction of mitophagy by starvation. Additionally, PpAtg32 was phosphorylated when mitophagy was induced. We found that PpAtg32 expression was suppressed by Tor and the downstream PpSin3-PpRpd3 complex. Inhibition of Tor by rapamycin induced PpAtg32 expression, but could neither phosphorylate PpAtg32 nor induce mitophagy. Based on these findings, we conclude that the Tor and PpSin3-PpRpd3 pathway regulates PpAtg32 expression, but not PpAtg32 phosphorylation.

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