Project description:Investigation of transcriptomic changes in M.luteus at 12hrs and 24hrs. Differences in fatty acid profiles of M. luteus at exponential and stationary phase is attributed to transcriptional changes of branched amino acid biosynthesis and degradation genes. This study is described by Pereira, J.H., E.B. Goh, J.D. Keasling, H.R. Beller and P.A. Adams in Crystal structure of FabH and factors affecting the distribution of branched fatty acids in Micrococcus luteus, which has been submitted to Acta Crystallographica Section D A 6 microarray study using total RNA recovered from six separate control cultures of Micrococcus luteus NCTC2665 strain with 3 harvested after 12hrs of growth and the other 3 after 24hrs of growth. Each chip measures the expression level of 2,374 ORF based on the draft genome sequence of Micrococcus luteus with ten 60-mer probe pairs (PM/MM) per gene, with 3-fold technical redundancy.
Project description:Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer’s disease (AD), and emerging evidence has shown that microRNAs (miRNAs) are alternative biomarkers and therapeutic targets for synaptic dysfunctions in AD. In this study, we found that the level of miR-431 was downregulated in the plasma of amnestic mild cognitive impairment (aMCI) and AD patients. In addition, it was decreased in the hippocampus and plasma of APPswe/PS1dE9 (APP/PS1) mice. Lentivirus mediated miR-431 overexpression in the hippocampus CA1 ameliorated synaptic plasticity and memory deficits of APP/PS1 mice, while it didn't affect the Aβ levels. Smad4 was identified as a target of miR-431, and Smad4 knockdown modulated the expression of synaptic proteins including SAP102, and protected against synaptic plasticity and memory dysfunctions in APP/PS1 mice. Furthermore, Smad4 overexpression reversed the protective effects of miR-431, indicating that miR-431 attenuated synaptic impairment at least partially by Smad4 inhibition. Thus, these results indicated that miR-431/Smad4 might be a potential therapeutic target for AD treatment.
