分子内結合が調節するJRABのLIMドメインによるアクチン細胞骨格の再編成

JRAB/MICAL-L2 is an effector protein of Rab13, a member of the Rab family of small GTPase. JRAB/MICAL-L2 consists of a calponin homology domain, a LIM domain, and a coiled-coil domain. JRAB/MICAL-L2 engages in intramolecular interaction between the N-terminal LIM domain and the C-terminal coiled-coil domain, and changes its conformation from closed to open under the effect of Rab13. Open-form JRAB/MICAL-L2 induces the formation of peripheral ruffles via an interaction between its calponin homology domain and filamin. Here, we report that the LIM domain, independent of the C-terminus, is also necessary for the function of open-form JRAB/MICAL-L2. In mechanistic terms, two zinc finger domains within the LIM domain bind the first and second molecules of actin at the minus end, potentially inhibiting the depolymerization of actin filaments (F-actin). The first zinc finger domain also contributes to the intramolecular interaction of JRAB/MICAL-L2. Moreover, the residues of the first zinc finger domain that are responsible for the intramolecular interaction are also involved in the association with F-actin. Together, our findings show that the function of open-form JRAB/MICAL-L2 mediated by the LIM domain is fine-tuned by the intramolecular interaction between the first zinc finger domain and the C-terminal domain

Association between Smoking during Pregnancy and Short Root Anomaly in Offspring

Short root anomaly (SRA) is a dental anomaly with short dental roots and its pathogenesis is poorly understood. This study investigated the association between maternal smoking during pregnancy and SRA in offspring. A survey was conducted on 558 children aged 8–16 years from two public schools in Ulaanbaatar, Mongolia. SRA was diagnosed using cases with a root-crown ratio of maxillary central incisors of ≤1.0. A questionnaire survey was conducted to assess maternal lifestyle habits. Multiple logistic regression was used to analyse the association between maternal smoking during pregnancy and SRA in offspring after adjusting for possible confounders. The prevalence of SRA in these children was 14.2%. Children whose mothers smoked from pregnancy to date were found to be 4.95 times (95% confidence interval [CI]: 1.65–14.79) more likely to have SRA than those whose mothers never smoked, after adjusting for possible confounders. Additionally, children whose mothers had been exposed to passive smoking during pregnancy were found to be 1.86 times (95% CI: 1.02–3.40) more likely to have SRA than those whose mothers had not been exposed to passive smoke. Our population-based study suggests that maternal and passive smoking exposure during pregnancy can affect tooth root formation in children

Changes in physical and chemical properties of archived sediment

http://www.godac.jamstec.go.jp/darwin/cruise/mirai/mr01-k03/