Hiroki Ono

Specific distribution patterns of hCDC47 expression in cutaneous diseases

hCDC47 is a human member of the MCM family, which has been implicated to be concerned with the regulatory machinery causing DNA to replicate once per cell cycle. In a previous paper, we described hCDC47 expression as being localized in the proliferative component of normal tissues, and showed greater expression in squamous cell skin carcinomas than in seborrheic keratosis. In the present study, we compared its expression in another type of skin tumor and variotis non‐neoplastic cutaneous proliferative diseases. Two patterns of distribution of hCDC47‐positive cells were observed. Keratoacanthomas showed a peripheral pattern in which only the cells located the basal cell layers were positive. Psoriasis vulgaris also showed this peripheral type of location, with the cells in the suprabasal layers also occasionally expressing hCDC47. Verruca vulgaris demonstrated a diffuse pattern, with positive epithelial cells distributed throughout the layers. Basal cell carcinomas also showed a similar pattern. The keratoacanthomas showed the highest hCDC47 positive cell rate (43.1%), followed by verruca vulgaris (42.5%). psoriasis vulgaris (23.4%), and basal cell carcinoma (17.3%). Our results suggest participation of hCDC47 in these proliferative disorders involving keratinocytes.

A Combined Case of Desmoplastic Trichoepithelioma and Nevus Cell Nevus

A 41‐year‐old woman with desmoplastic trichoepithelioma associated with pigmented nevus presented. Pigmented nevus had been present on her face at birth. She had received cryotherapy and dermabrasion at a small part of the pigmented nevus. As a result of the therapy, the discoloration disappeared. The lesion lately increased and became hard. Histologically, the lesion was composed of two distinctive but intimately mixed cellular components; nevus cells and basaloid cells. In the pigmented lesion, basaloid cells were not present. To our knowledge, this is the first reported case of desmoplastic trichoepithelioma associated with nevocellular nevus in Japan.

The MinD homolog FlhG regulates the synthesis of the single polar flagellum of Vibrio alginolyticus

FlhG, a MinD homolog and an ATPase, is known to mediate the formation of the single polar flagellum of Vibrio alginolyticus together with FlhF. FlhG and FlhF work antagonistically, with FlhF promoting flagellar assembly and FlhG inhibiting it. Here, we demonstrate that purified FlhG exhibits a low basal ATPase activity. As with MinD, the basal ATPase activity of FlhG can be activated and the D171A residue substitution enhances its ATPase activity sevenfold. FlhG‐D171A localizes strongly at the cell pole and severely inhibits motility and flagellation, whereas the FlhG K31A and K36Q mutants, which are defective in ATP binding, do not localize to the poles, cannot complement a flhG mutant and lead to hyperflagellation. A strong polar localization of FlhF is observed with the K36Q mutant FlhG but not with the wild‐type or D171A mutant FlhG. Unexpectedly, an Ala substitution at the catalytic residue (D60A), which abolishes ATPase activity but still allows ATP binding, only slightly affects FlhG functions. These results suggest that the ATP‐dependent polar localization of FlhG is crucial for its ability to downregulate the number of polar flagella. We speculate that ATP hydrolysis by FlhG is required for the fine tuning of the regulation.