Medial-apical actomyosin
In addition to the band of circumferential actomyosin associated with junctions there another actomyosin network that produces mechanical forces in epithelial tissues. Probably because it is less conspicuous than junction actomyosin it took much longer for researchers to appreciate importance of medial-apical actomyosin network (Fig. 1.10), in fact even when it was directly observed it the more prominent purse string model was still favored. The protein Shroom 3 was first characterized near the turn of the millennia to induce apical constriction for neural tube closure in both mice and frog \cite{Haigo2003,Hildebrand1999,Nishimura2008}. Interestingly, the proposed mechanism for Shoorm 3 induced apical constriction was the accumulations of actomyosin around the circumference of cells even though both junctional and medial apical actomyosin increased \cite{Haigo2003,Nishimura2008}. Medial-apical actomyosin was first appreciated for its role in apical constriction when live imaging was performed on gastrulating Drosophila \cite{Martin2009}.  Where the researches found that temporal burst of Myosin II accumulated medial-apically to induce apical constriction in a pulsed contraction. Outside of morphogenic events such as apical constriction medial-apical actomyosin has been shown to be a load bearing structure in stable epithelia \cite{Ma_2009}. Laser hole drilling of both junctional and medial-apical F-actin revealed that epithelia acts more as continuous mechanical sheet rather than an array of contractile vertices \cite{Ma_2009}. Even with with these findings epithelial tissues are still often thought of as an array of contractile vertices and conclusions are made assuming the mechanical strain is stored only in circumferential actomyosin. Medial-apical and junctional are distinct, but also very similar. There are still many unanswered question about the function of medial-apical actomyosin and it's interplay with circumferential actomyosin. How are they controlled and regulated and differentiated, does one feed into the other, etc. My third chapter shows that the scaffolding protein Anillin dramatically increased medial-apical actomyosin and this leads to dramatic changes in the mechanics of epithelial cells.