Mycosis is an infection to human caused by fungi, such as mold and yeast. Among mycosis, deep mycosis which infects organs and tissues, has become a particularly serious problem. To treat those deep mycosis, chemotherapy with antifungal agents is used. However, the types of antifungals are few and the treatment options are limited. Since fungi and humans have similar cell structures, existing antifungal agents have also been reported to have side effects on humans. Furthermore, the emergence of resistant fungi has become a problem due to the long-term use of the drug.From those problems, development of an antifungal agent having a new mechanism of action is required. Therefore, our laboratory focused on tip growth, a growth method specific to fungi. Tip growth elongates the cell by repeating the decomposition and synthesis of the cell wall (β-1,3-D-Glucan). It has been reported that the cell wall-degrading enzyme β-1,3-D-Glucanase (BGL2) involved in this tip growth is vesicular transported from the inside of the cell to the growth point. We consider that targeting vesicle transport during tip growth will provide selective toxicity to fungi. The purpose of this study is to develop novel antifungal agents targeting vesicle transport during fungal tip growth. An evaluation system for visualizing vesicle transport was constructed by fusing green fluorescent protein GFP downstream of BGL2 to be transported to the growth point by expression of the protein in Saccharomyces cerevisiae (the results of the localization were shown in Fig.1).Using this evaluation system, vesicle transport inhibitory activity was screened for 100 kind herbal medicine extract. As a result, vesicle transport inhibitory activity was observed in 8 types.In addition, we attempted to construct a similar evaluation system using Candida albicans and aimed to evaluate fungi that form hyphae that cause actual mycosis.Fig.1 Confocal laser scanning microscope image of an evaluation system for antifungal compounds using S. cerevisiae.(a) Localization of BGL2-EmGFP to growth point.(b) Localization of BGL2-EmGFP to the division site.(C) Intracellular distribution of BGL2-EmGFP treated with vesicle transport inhibitor. Figure 1