遺伝子と栄養の相互作用における樹状突起形成のメカニズム解明

2013 Fiscal Year Annual Research Report

• Project/Area Number: 13F03798
• Research Institution: The Institute of Physical and Chemical Research
• Principal Investigator: MOORE Adrian 独立行政法人理化学研究所, 脳科学総合研究センター, チームリーダー (30442932)
• Co-Investigator(Kenkyū-buntansha): マッキ マーク 独立行政法人理化学研究所, 脳科学総合研究センター, 外国人特別研究員
• Project Period (FY): 2013 – 2015
• Keywords: Dystrophin / actin cytoskeleton / bactcria / environment / sensory neurons

Outline of Annual Research Achievements

We hypothesis that a Dystrophin dependent mechanism controls dendrite development in response to an environmental factor. We have successfully shown that Dystrophin controls dendrite growth of sensory neurons. Our data demonstrates that Dystrophin in those neurons represses branching event. Then, we showed that the dendrite growth of sensory neuron was affected when the fly food's quality was changed. We also demonstrated that the mechanism controlling the dendrite growth in response to the fly food's quality is Dystrophin dependent. At larval stage, larvae feed often to get nutrients which are essential for the growth. Therefore, we expected that the food quality affecting the dendrite growth of sensory neuron were the nutrients. However, our data suggest that other factor in the fly food can affect the dendrite growth of sensory neurons : the bacteria. Our preliminary data suggest that a Dystrophin dependent mechanism controls dendrite development in response to the bacterial infection. Now, we are trying to set up protocols allowing us to investigate in details this interaction between bacteria and dendrite growth.

Current Status of Research Progress

2: Research has progressed on the whole more than it was originally planned.

Reason

As we mentioned in Outline of the Research Result, our research is progressing successfully.

Strategy for Future Research Activity

We will determine how bacteria alter dendrite growth through a dystrophin dependent mechanism. First, we would like to understand how sensory neurons are able to sense bacteria from the environment. Do those neurons bind directly bacteria? Do sensory neurons sense a general bacterial infection state? Sensory neurons are in contact to the hemolymph (larval body fluid), however it's unclear if bacteria can invade the hemolymph or not. Therefore, we will make by our self GFP-labelled bacteria (fluorescent bacteria) in order to track, after infection, fluorescent bacteria in live imaging. Thanks to those experiments, we will know if bacteria can invade the hemolymph or not. In parallel, we will try to know if sensory neurons sense bacterial infection through the systemic immune response. In the hemolymph, sensory neurons are in contact to the hemocytes, which are essential to induce a systemic immune response. So we would like to know if the bacterial infection sensing by sensory neurons is dependent to the hemocytes. We will block the systemic immune response of the larvae, in using transgenic flies, and check if dendrite growth of sensory neurons can still be affected after bacterial infection. We also planned to discover in details the dystrophin dependent mechanisms controlling the dendrite growth in response to bacterial infection. For that, we will set up several genetic interactions experiments.