A Study on the Origin of Peroxisomes: Possibility of Actinobacteria Symbiosis

The origin of peroxisomes as having developed from the endoplasmic reticulum (ER) was proposed on the basis of the similarity between some peroxisomal proteins and ER proteins, and the localization of some peroxisomal proteins on the ER. To study the evolutionary distance between peroxisomes and ER and Prokaryotes, we carried out a phylogenetic analysis of CDC48 (cell division control 48) and its homologs, including ER-localized CDC48, CDC48 homologs in Prokaryotes and peroxisome-localized PEX1 and PEX6. A similarity search analysis of peroxisomal protein sequences to prokaryotic protein sequences using BLAST at several thresholds (E-values) was also done. We propose Actinobacteria symbiosis for the origin of peroxisomes based on the following evidence: (1) PEX1 and PEX6 are close in distance to CDC48 homologs in Actinobacteria, and these distances are closer than to ER-localized CDC48. (2) Actinobacteria proteins show the highest degree of similarity to peroxisomal proteins compared with other prokaryotes

A tripartite paternally methylated region within the Gpr1-Zdbf2 imprinted domain on mouse chromosome 1 identified by meDIP-on-chip

The parent-of-origin specific expression of imprinted genes relies on DNA methylation of CpG-dinucleotides at differentially methylated regions (DMRs) during gametogenesis. To date, four paternally methylated DMRs have been identified in screens based on conventional approaches. These DMRs are linked to the imprinted genes H19, Gtl2 (IG-DMR), Rasgrf1 and, most recently, Zdbf2 which encodes zinc finger, DBF-type containing 2. In this study, we applied a novel methylated-DNA immunoprecipitation-on-chip (meDIP-on-chip) method to genomic DNA from mouse parthenogenetic- and androgenetic-derived stem cells and sperm and identified 458 putative DMRs. This included the majority of known DMRs. We further characterized the paternally methylated Zdbf2/ZDBF2 DMR. In mice, this extensive germ line DMR spanned 16 kb and possessed an unusual tripartite structure. Methylation was dependent on DNA methyltransferase 3a (Dnmt3a), similar to H19 DMR and IG-DMR. In both humans and mice, the adjacent gene, Gpr1/GPR1, which encodes a G-protein-coupled receptor 1 protein with transmembrane domain, was also imprinted and paternally expressed. The Gpr1-Zdbf2 domain was most similar to the Rasgrf1 domain as both DNA methylation and the actively expressed allele were in cis on the paternal chromosome. This work demonstrates the effectiveness of meDIP-on-chip as a technique for identifying DMRs

The Dichotomous Pattern of IL-12R and IL-23R Expression Elucidates the Role of IL-12 and IL-23 in Inflammation

IL-12 and IL-23 cytokines respectively drive Th1 and Th17 type responses. Yet, little is known regarding the biology of these receptors. As the IL-12 and IL-23 receptors share a common subunit, it has been assumed that these receptors are co-expressed. Surprisingly, we find that the expression of each of these receptors is restricted to specific cell types, in both mouse and human. Indeed, although IL-12Rβ2 is expressed by NK cells and a subset of γδ T cells, the expression of IL-23R is restricted to specific T cell subsets, a small number of B cells and innate lymphoid cells. By exploiting an IL-12- and IL-23-dependent mouse model of innate inflammation, we demonstrate an intricate interplay between IL-12Rβ2 NK cells and IL-23R innate lymphoid cells with respectively dominant roles in the regulation of systemic versus local inflammatory responses. Together, these findings support an unforeseen lineage-specific dichotomy in the in vivo role of both the IL-12 and IL-23 pathways in pathological inflammatory states, which may allow more accurate dissection of the roles of these receptors in chronic inflammatory diseases in humans

Attenuator

PROBLEM TO BE SOLVED: To provide an attenuator that has higher linearity and a satisfactory frequency characteristic.SOLUTION: A resistance that is subject to the same process fluctuation as a resistance included in an attenuation section 10a is disposed in a correction circuit 10c, a process fluctuation is detected on the basis of the resistance of the correction circuit 10c, and in accordance with the process fluctuation, a control signal to the attenuation section 10a from an attenuation control circuit 10b is adjusted such that a distortion component caused on a signal line and a distortion component caused on a short circuit line match in magnitude. Even when the resistance included in the attenuation section 10a shows a process fluctuation, the distortion component caused on the signal line and the distortion component caused on the short circuit line can match in magnitude to exert the effect of canceling both distortion components