MIG-10, an Adapter Protein, Interacts with ABI-1, a Component of Actin Polymerization Machinery

MIG-10 is a protein known to be involved in axon guidance and neuronal migration in early development in C. elegans. In an effort to better understand the protein's function, this project used the yeast two hybrid system to screen a cDNA library (representing the entire C. elegans genome) for proteins with which MIG-10 interacts. The idea is if we can associate it with proteins of known function, we'll have a better idea as to what MIG-10 itself does. Our research revealed that MIG-10 interacts with (among other proteins) ABI-1, which is a component of actin polymerization machinery. In general, development of the nervous system requires an extraordinarily dynamic array of signaling molecules and transduction pathways. This stems from the fact that proper nervous system function relies on the formation of specific connections between varying neuronal cell types (Bear et al., 2007). The migration of axons and cell bodies necessary to achieve these connections will occur during and beyond embryonic development. The migration path of each neuron is dependent on a variety of extra cellular cues, providing information about the immediate environment. Biomolecules, such as netrin, slit, ephrin and semaphorin, have already been indicated as signaling compounds in vertebrates, C. elegans and D. melanogaster (Yu and Bargman, 2001). These signals then act on a variety of receptors, eliciting a signal cascade that may lead to actin polymerization, depolymerization, or other fundamental cellular processes. In some cases signal molecules can have a variety of responses (Disanza et al, 2005). Depending on the cell, receptor, or cellular localization, these signals can alter the migration pattern of a cell or axon in a concentration gradient dependent manner. In C. elegans there are a number of important players involved in these processes; one of them is mig-10 (Quinn et. al, 2006). It was a screen for defective neuronal migration that led to mig-10's discovery (Manser, 1990). Several recessive mutations of the mig-10 gene have been shown to cause abnormal cell migration in multiple types of neurons and deformities in excretory cell outgrowth (Manser et al., 1997). It is currently thought that the MIG-10 protein mediates the anterior posterior guidance/migration system for these cells. Additionally, it has been found that axonal guidance can be enhanced by the over-expression of mig-10 (Quinn, Ryder, et al, 2006). When MIG-10 is expressed in HEK293 cells, it co-localizes with filamentous actin and creates fillipodial protrusions (Quinn et al., 2006). Additionally, …