Graduate School of Frontier Biosciences, Osaka University

Japanese

Colloquium 205

Speaker Maho Hamasaki (Associate Prof.(FBS Laboratpry of Intracellular Membrace Cynamics(Yoshimori Lab.)))
Title lysophagy: How the damaged membrane is removed & mechanistic insight of LC3-II lipidation
Speaker Gota Yoshida (PhD student (Dep. Genetics (Yoshimori Lab.)))
Title Rubicon negatively regulates osteoblast differentiation
Date Wed., JAN. 30, 2019, 12:15~13:00
Place 2F Seminar room, BioSystems Building
Host Contact:Maho Hamasaki
Tel :0668794856
E-mail:hamasaki@fbs.osaka-u.ac.jp

Title/Abstract

lysophagy: How the damaged membrane is removed & mechanistic insight of LC3-II lipidation

Autophagy is induced when cells are starved and also when cells need cleaning. We will introduce the latter type of autophagy, especially lysophagy which clears damaged lysosomes. Lysosomes can be damaged by cells taken up cholesterol crystals, ureic acid crystals and other irritable particles that can be a causative of life style diseases. We will introduce our recent finding on how damaged lysosomes are removed. Also, we will introduce our recent findings on LC3 proteins and putative drug that is effective on cell cleaning type of autophagy.

Rubicon negatively regulates osteoblast differentiation

We have previously reported Rubicon negatively regulates autophagy. However, the physiological roles of Rubicon remain elusive in vivo. We now investigate the role of Rubicon in bones by generating osteoblast specific Rubicon deficient mice. We generated conditional knock out mice {Osterix-Cre/Rubicon (flox/flox)} that lack Rubicon in osteoblast. Osterix-Cre/Rubicon (flox/flox) mice progressively developed skeletal abnormalities in femur bones. In addition, Rubicon deficient osteoblast exhibited increased differentiation, mineralization and expression levels of transcription factors, such as Runx2 and Osteocalcin that are master regulators of osteoblast. Furthermore, Notch, negative regulator of osteoblast, signaling downstream transcription factors such as HeyL, Hes1 and Hes3 were expressed at lower levels in Rubicon deficient osteoblast. Consistently, we found reduction the protein expression of Notch receptor due to upregulation of autophagic flux in Rubicon deficient osteoblast. These data suggested that Notch receptor could be degraded by autophagy or reduced by other mechanisms, and now we are investigating the Notch receptor degradation mechanisms. よろしくお願いいたします。


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