Front cover: Flow cytometry is a technology that allows high throughput analysis of the characteristics of cell populations by optically and rapidly measuring the morphological characteristics and fl uorescent signals of the cells suspended in a narrow stream of fl uid in equipment (fl ow cytometer). In addition, the equipment with a cell sorter can collect a certain type of cells from a heterogeneous population by charging droplets containing such cells identifi ed by the optical data and attracting them by an electrostatic defl ector. In this post town in this drawing, ‘Positive’ inn on the right and ‘Negative’ inn on the left are finding and attracting potential customers from passersby. They just look like a cell sorter. There is seen above them a cluster of clouds that resembles flow cytometric data. Designed by TRAIS Co., Ltd. (Kobe, Japan).

Group photograph from the Conference on Transposition and Genome Engineering 2015 (TGE 2015) held at Nara Kasugano International Forum—IRAKA—in Nara, Japan on 17 to 20 November 2015.

Mitochondria are dynamic organelles, but mechanism regulating balance between fusion and fission has not been clarified. In mitochondrial fission-deficient cells, mitochondrial fusion proteins were repressed. Mitofusins are degraded via ubiquitin-proteasome system mediated by BAT3, and L-OPA1 was processed via OMA1. Thus, distinct types of protease systems are involved in the homeostatic regulation of mitochondrial morphology.

Dll1–Notch interaction promotes Mib1 ubiquitin ligase activity, and Dll1 is ubiquitinated by Mib1. The Mib1 ubiquitin ligase activity modulates the recruitment of dynamin 2 via Snx18 to the sites of Dll1 internalization and promotes Dll1 endocytosis. This process leads to mechanical dissociation of the NotchECD and the release of the NICD in adjacent cells.

Organ identity specification factor, Winged-Eye (WGE), localized to specific nuclear foci called the histone locus body (HLB), an evolutionarily conserved nuclear body required for S phase-specific histone mRNA production. We propose that WGE at HLB contributes to genomic stability and development by regulating heterochromatin structure via histone gene regulation.

SKIP is a PIP₃ phosphatase that negatively regulates insulin signaling. SKIP directly binds to GRP78 through the SKICH domain, which is necessary for the localization of SKIP at ER. Dissociation from GRP78 on insulin stimulation allows SKIP to bind to Pak1 at the plasma membrane.

In this study, we found that trans-activation response (TAR) DNA-binding 43-kDa protein (TDP-43), recognizes G-quadruplex-containing mRNAs and transports them up to neurites for local translation. The success was based on the first purification of TDP-43 in soluble dimer forms, allowing in vitro SELEX screening of target RNA molecules. Furthermore, we found that the loss-of-function mutation or over-expression of TDP-43 result in defect of intracellular transport of mRNAs in neural cells, thereby leading to the neurodegenerative disorder such as amyotrophic lateral sclerosis and frontotemporal lobar degeneration.

The specific interaction of Ctf18-RFC with Polε is a conserved feature between these proteins. We demonstrated that the interaction plays a crucial role in maintaining genome stability in budding yeast, probably through recruitment of this PCNA loader to the replication fork.

The adenohypophysis (AH), the anterior part of the pituitary gland, consists of six types of hormone-secreting cells and their cell fate is regulated by several signaling pathway during animal development. We found that Notch signaling is necessary for AH cell specification in wider time range than previously reported in zebrafish. We also found, by using knockdown and knockout zebrafish embryos, that multiple downstream effectors, including Her4.1 and Hey1, are likely to mediate Notch signaling during AH cell specification.

We found that the addition of serine, a chemotactic attractant, to a PomB(L160C/I186C) mutant restored motility without cleaving the disulfide bridge in Vibrio. Motility was restored without serine in Che⁻ mutants. We speculate that serine changed the rotor conformation to suppress the motor function of the PomB mutation.

Model for the role of the FBXL12-ALDH3 axis in T-cell differentiation. FBXL12 mediates ubiquitin-dependent degradation of ALDH3 and thereby promotes the differentiation of DP cells into CD4 SP or CD8 SP cells.