The receptor-like cytoplasmic kinase CDG1 negatively regulates Arabidopsis pattern-triggered immunity and is involved in AvrRpm1-induced RIN4 phosphorylation.

Arabidopsis CDG1 negatively regulates flg22- and chitin-triggered immunity by promoting FLS2 and CERK1 degradation and is partially required for bacterial effector AvrRpm1-induced RIN4 phosphorylation. Negative regulators play indispensable roles in pattern-triggered immunity in plants by preventing sustained immunity impeding growth. Here, we report Arabidopsis thaliana CONSTITUTIVE DIFFERENTIAL GROWTH1 (CDG1), a receptor-like cytoplasmic kinase VII member, as a negative regulator of bacterial flagellin/flg22- and fungal chitin-triggered immunity. CDG1 can interact with the flg22 receptor FLAGELLIN SENSITIVE2 (FLS2) and chitin co-receptor CHITIN ELICITOR RECEPTOR KINASE1 (CERK1). CDG1 overexpression impairs flg22 and chitin responses by promoting the degradation of FLS2 and CERK1. This process requires the kinase activity of MEK KINASE1 (MEKK1), but not the Plant U-Box (PUB) ubiquitin E3 ligases PUB12 and PUB13. Interestingly, the Pseudomonas syringae effector AvrRpm1 can induce CDG1 to interact with its host target RPM1-INTERACTING PROTEIN4 (RIN4), which depends on the ADP-ribosyl transferase activity of AvrRpm1. CDG1 is capable of phosphorylating RIN4 in vitro at multiple sites including Thr166 and the AvrRpm1-induced Thr166 phosphorylation of RIN4 is diminished in cdg1 null plants. Accordingly, CDG1 knockout attenuates AvrRpm1-induced hypersensitive response and increases the growth of AvrRpm1-secreting bacteria in plants. Unexpectedly, AvrRpm1 can also induce FLS2 depletion, which is fully dependent on RIN4 and partially dependent on CDG1, but does not require the kinase activity of MEKK1. Collectively, this study reveals previously unknown functions of CDG1 in both pattern-triggered immunity and effector-triggered susceptibility in plants.

LPS priming before plaque deposition impedes microglial activation and restrains Aß pathology in the 5xFAD mouse model of Alzheimer's disease.

Microglia have an innate immunity memory (IIM) with divergent functions in different animal models of neurodegenerative diseases, including Alzheimer's disease (AD). AD is characterized by chronic neuroinflammation, neurodegeneration, tau tangles and ß-amyloid (Aß) deposition. Systemic inflammation has been implicated in contributing to the progression of AD. Multiple reports have demonstrated unique microglial signatures in AD mouse models and patients. However, the proteomic profiles of microglia modified by IIM have not been well-documented in an AD model. Therefore, in the present study, we investigate whether lipopolysaccharide (LPS)-induced IIM in the pre-clinical stage of AD alters the microglial responses and shapes the neuropathology. We accomplished this by priming 5xFAD and wild-type (WT) mice with an LPS injection at 6 weeks (before the robust development of plaques). 140 days later, we evaluated microglial morphology, activation, the microglial barrier around Aß, and Aß deposition in both 5xFAD primed and unprimed mice. Priming induced decreased soma size of microglia and reduced colocalization of PSD95 and Synaptophysin in the retrosplenial cortex. Priming appeared to increase phagocytosis of Aß, resulting in fewer Thioflavin S+ Aß fibrils in the dentate gyrus. RIPA-soluble Aß 40 and 42 were significantly reduced in Primed-5xFAD mice leading to a smaller size of MOAB2+ Aß plaques in the prefrontal cortex. We also found that Aß-associated microglia in the Primed-5xFAD mice were less activated and fewer in number. After priming, we also observed improved memory performance in 5xFAD. To further elucidate the molecular mechanism underlying these changes, we performed quantitative proteomic analysis of microglia and bone marrow monocytes. A specific pattern in the microglial proteome was revealed in primed 5xFAD mice. These results suggest that the imprint signatures of primed microglia display a distinctive phenotype and highlight the potential for a beneficial adaption of microglia when intervention occurs in the pre-clinical stage of AD.

The first complete chloroplast genome of Pteris vittata (Pteridaceae), an arsenic hyperaccumulating fern.

It is the first report on complete chloroplast genome of Pteris vittata, an arsenic hyperaccumulating fern. Its genome size is 154,130 bp, with a typical circular structure including a large single-copy (LSC) (82,623 bp) and a small single-copy (SSC) (20,957 bp) regions separated by a pair of inverted repeats (25,275 bp each). The plastome encodes 132 genes, including 87 protein-coding genes, 35 tRNA genes, eight rRNA genes, and two pseudogenes. The overall Guanine+Cytosine (GC) content is 41.7% and GC content in the IR regions is higher than in the LSC and SSC regions. Maximum likelihood (ML) tree indicated that P. vittata was clustered with Ceratopteris richardii.