Martinez-Arias Lab
Department of Genetics, University of Cambridge
Fan Cheung Wu
PhD student
fc272@cam.ac.ukDepartment of Genetics,
Downing Street, Cambridge
CB2 3EH,England
Telephone: +44 1223 766595
Fax: +44 1223 333992
I completed my undergradute degree here, at the University of Cambridge, where I studied the Natural Sciences Tripos, specializing in Genetics during my Part II year, from which I graduated in 2007. During my Part II I worked under both Dr. Nicole Gorfinkiel and Prof. Alfonso Martinez-Arias’ supervision, and it was then when I began to show interest in the complex process of morphogenesis. In particular how cells are capable of integrating the vast amount of signals and information they receive, process it and generate an output which may involve the activation of other genes and/or cause dramatic rearrangements in cell shape, which for this function ultimately give way to cell sheet rearrangements and thus, morphogenesis.
I started my PhD in the Martinez-Arias lab in Michaelmas of 2007 working in the morphogenesis branch of the lab. My aim in this PhD is to try and identify possible interactions between Notch and JNK signaling, using dorsal closure as the model system. This project arises from previous work done in the lab where they have shown that during dorsal closure, deficiency of Notch rescues the dorsal hole phenotype that is displayed in mutants that lack JNK signaling.
In these last two years I have been focusing on trying to understand the mechanics of this observation using a combination of classic genetic rescues, immunostainings and in vivo imaging of embryos. For clues in this process I have been looking into the dynamic changes in the cytoskeleton, which is a major player that is crutial for closure of the dorsal hole (fig. 1&2). Subsequently I have tried to disect the interaction between the two signaling pathways by focusing on different aspects of Notch biology, such as its canonical function, it’s trafficking role (movie 1) and its function as a receptor of the Delta ligand. Finally, the study of this interaction between Notch and JNK is of appeal because it builds on the growing hypothesis which suggests that individual signaling pathways are likely to form part of a “network” of signaling events, rather than being isolated sequences of activations and suppressions.
Fig.1. Immunostainings of F-actin in wild type, hemipterous and loss-of-function Notch backgrounds illustrating the difference in F-actin stalibility. Arrows indicate the lack of actin nucleating centres in the hemipterous embryo (pink arrow), which are quite prominent in the wild type (white arrow)
Please click on the image for larger version
Fig.2. Alpha and beta tubulin stainings in wild type, hemipterous, Notch and the Notch hemipterous double mutant illustrating the stability of polimerized tubulin in the different genetic backbrounds. Arrows indicate the extent of tubulin polimerization, in the wild type it spans the dormal most epidermal cells, in the hemipterous only half way down the dorsal most epidermal cell and in both the Notch and the Notch hemipterous it spans down to the lateral epidermis.
Please click on the image for larger version