Lu Liu

Cyclin-dependent kinase 5 has been implicated in Alzheimer's disease pathogenesis. Here, we demonstrate that overexpression of p25, an activator of cdk5, led to increased levels of BACE1 mRNA and protein in vitro and in vivo. A p25/cdk5 responsive region containing multiple sites for signal transducer and activator of transcription was identified in the BACE1 promoter. STAT3 interacts with the BACE1 promoter, and p25-overexpressing mice had elevated levels of pSTAT3 and BACE1, whereas cdk5-deficient mice had reduced levels. Furthermore, mice with a targeted mutation in the STAT3 cdk5 responsive site had lower levels of BACE1. Increased BACE levels in p25 overexpressing mice correlated with enhanced amyloidogenic processing that could be reversed by a cdk5 inhibitor. These data demonstrate a pathway by which p25/cdk5 increases the amyloidogenic processing of APP through STAT3-mediated transcriptional control of BACE1 that could have implications for AD pathogenesis

The thin set theorem for n-tuples and k colors states that every k-coloring of $[\mathbb {N}]^n$ admits an infinite set of integers H such that $[H]^n$ avoids at least one color. In this paper, we study the combinatorial weakness of the thin set theorem in reverse mathematics by proving neither $\operatorname {\mathrm {\sf {TS}}}^n_k$, nor the free set theorem imply the Erdős–Moser theorem whenever k is sufficiently large. Given a problem $\mathsf {P}$, a computable instance of $\mathsf {P}$ is universal iff its solution computes a solution of any other computable $\mathsf {P}$ -instance. It has been established that most of Ramsey-type problems do not have a universal instance, but the case of Erdős–Moser theorem remained open so far. We prove that Erdős–Moser theorem does not admit a universal instance.

© 2016 American Society of Plant Biologists. All rights reserved.Calcium/calmodulin-dependent protein kinase has been shown to play an important role in abscisic acid -induced antioxidant defense and enhance the tolerance of plants to drought stress. However, its downstream molecular events are poorly understood. Here, we identify a NAC transcription factor, ZmNAC84, in maize, which physically interacts with ZmCCaMK in vitro and in vivo. ZmNAC84 displays a partially overlapping expression pattern with ZmCCaMK after ABA treatment, and H2O2 is required for ABA-induced ZmNAC84expression. Functional analysis reveals that ZmNAC84 is essential for ABA-induced antioxidant defense in a ZmCCaMK-dependent manner. Furthermore, ZmCCaMK directly phosphorylates Ser-113 of ZmNAC84 in vitro, and Ser-113 is essential for the ABA-induced stimulation of antioxidant defense by ZmCCaMK. Moreover, overexpression of ZmNAC84 in tobacco can improve drought tolerance and alleviate drought-induced oxidative damage of transgenic plants. These results define a mechanism for ZmCCaMK function in ABA-induced antioxidant defense, where ABA-produced H2O2 first induces expression of ZmCCaMK and ZmNAC84 and activates ZmCCaMK. Subsequently, the activated ZmCCaMK phosphorylates ZmNAC84 at Ser-113, thereby inducing antioxidant defense by activating downstream genes.