A lack of in vivo models has hampered insight into the mechanisms driving cell-invasive behavior. The behavior of a single uterine cell in Caenorhabditis elegans called the anchor cell (AC) provides such an in vivo model, allowing for easy visualization and genetic manipulation. During normal development in the C. elegans hermaphrodite, the AC invades through the underlying juxtaposed uterine and ventral epidermal basement membranes (BM) to establish the initial uterine-vulval contact. In addition to the genetic tractability and ease of visualization, the consistency of this event, occurring at the same time in every wild-type hermaphrodite, makes for a powerful model of cell invasion. We have established an in vivo system to visualize anchor cell invasion as it occurs in real time using a laminin-GFP fusion (LAM-1::GFP, Kao and Wadsworth 2006, Dev Biol. 290(1): 211-219) or a hemicentin-GFP fusion (GFP-hemicentin, Vogel and Hedgecock 2001, Development 128(6): 883-894), both markers of the BM, in combination with a PH::mCherry (PH domain from PLC?, a gift from Anjon Audhya) driven by an AC-specific promoter, labeling the invasive membrane (Sherwood et al. 2005, Cell 121(6): 951-962). To investigate the real-time dynamics of invasion, we have begun to characterize AC invasion in wild-type animals. Prior to invasion there is a deposition of GFP-hemicentin and an apparent increase of LAM-1::GFP in the uterine BM directly below the AC, suggesting that the AC deposits or recruits additional BM components, prior to migration through it. Invasion appears to initiate with a single filopod extending through a tiny hole in the BM. Once this filopodial process reaches through the BM, possibly contacting vulval cells below, it begins to widen, often fanning out on the ventral side of the BM. This widening of the AC extension seems to be coincident with widening of the hole in the BM, as visualized by LAM-1::GFP. The initial characterization of wild-type invasion has brought about several questions. 1) How is the initial filopod generated, and how does it penetrate through the BM? 2) What dictates the precise location of the initial protrusive filopod? 3) What happens to the BM under the AC as the filopod widens? 4) Do other BM components similarly increase under the AC, how are they recruited there, and what function does their increase serve? It is our hope that through a detailed cell-biological analysis, in combination with genetic screens and mutant analysis, that we will gain insight into these questions and lead to a better understanding of the mechanisms that endow invasive cells with the ability to traverse basement membranes.