On giant's shoulders: an interview with Masatoshi Takeichi (RIKEN Center for Developmental Biology, Kobe).

Abstract

Masatoshi Takeichi independently discovered the cadherin adhesion molecules in 1977. He followed this with many seminal papers that elucidated the role of these molecules in disease, and defi ned the capacity for their dysfunction to contribute to disease. In the course of this work he has fl uently moved between cellular and developmental models and several fi elds of biology. His early scientifi c training, and the background to those early achievements, have been eloquently documented before (Takeichi, 2004) . In this recent interview, we therefore decided to focus more on his current interests and his thoughts for the future. ASY: Takeichi-sensei, you and your lab work in many areas of biology. Only in this past year (2012), you have published papers that range from the role of planar cell polarity in neural tube closure (Nishimura et al., 2012) to regulation of microtubule organization (Tanaka et al., 2012). Is there a central theme that you use to guide your work? Takeichi: Thank you for the fi rst, critical question. Yes, I admit that the papers from my lab in the last year dealt with diverse subjects. However, all the subjects originated in my studies on cell – cell adhesion. The neural tube study tried to solve the problem of how the cadherin-mediated cell junctions contract in a biased direction for bending the neural plate. The microtubule minus end-binding protein Nezha/CAMSAP3 was identifi ed through our previous study aimed at analyzing the function of p120-catenin bound to cadherins (Meng et al., 2008). Actually I have been trying to restrict my research subjects to the problems of cell – cell contact and recognition, and related developmental or pathogenic phenomena. With this specifi c line of interests, I have been fully enjoying my life as a cell and developmental biologist. However, I am now slightly changing this tradition of my research, as I feel a lot of fun with the analysis of Nezha/CAMSAP3. I realized the fi eld of microtubule minus ends to be a sort of niche, and so I am quite excited to fi ll the niche. And I feel an attachment to Nezha/CAMSAP3, similar to that I had to cadherin at the time when I discovered it. My lab is being split into subgroups studying cell adhesion and microtubules. This could be a stupid choice, particularly for a lab which I am trying to downsize considering my age. I am also experiencing diffi culty in publishing papers on the subjects with which I am unfamiliar. This is just like what happened when I was young. Nevertheless, I have decided to take this challenge, as I could be able to make another contribution to life sciences. ASY: So, if we talk about cell adhesion for the time being, what are the issues that most interest you at the moment? Takeichi: I am consistently interested in cell behavior underlying the “ self-organization of tissues ” . As a number of classic studies have shown, animal cells are capable of autonomously organizing tissues. I believe that this is the fundamental ability for animal cells, and understanding its molecular basis should lead us to answer the general question of how our bodies are formed. More recently, Yoshiki Sasai in our institute demonstrated that ES cell-derived neuroepithelial cells can self-organize brain cortices and even the entire optic cup, confirming that individual cells know how to organize tissues without any external instructions. Cell adhesion regulators should take part in such processes. Along this line of my interest, my lab is carrying out a couple of studies. For example, we recently showed that PCP signals mediated by a Celsr (Flamingo) cadherin control the polarized contraction of adherens junctions, and, in turn, neural plate bending (Nishimura et al., 2012). This is, I believe, a conceptually important finding, as morphological changes occurring in individual cells determine the global pattern of the tissues to which these cells belong. We are continuing this study to find out how Celsr is recruited to particular cell junctions, and how actin regulators respond to Celsr signals. Cell Communication & Adhesion, 20: 147–149, 2013 © 2013 Informa Healthcare USA, Inc. ISSN: 1541-9061 print / 1543-5180 online DOI: 10.3109/15419061.2013.854333