A molecular model for linear and lateral growth of type I collagen fibrils.
A model is proposed for Type I collagen fibrillogenesis in which linear and lateral growth are directed by attractive charged pair interactions. It is suggested that linear growth decreases the rate of rotational motion resulting in an increased rate of lateral collisions. The mechanism of linear aggregation involves interactions between sets of unusual charged pairs located at positions 53, 54 and 56 and positions 990 and 992 as well as in the non-helical ends. These charged pairs attract each other electrostatically as well as form a hydrophobic pocket between the molecules. Lateral growth occurs by attractions between D-staggered, charged pairs which alternate between intra- and interchain states. Interchain interactions lead to lateral association of neighboring molecules and formation of a D-staggered unit containing five trimers. Rotational motion of the triple-helical backbone as well as the ability of charged pairs in their interchain state to interact by several different possible combinations between alpha-chains suggest that lateral packing of collagen molecules into fibrils at least in vitro may not need to be specific.
D000595:Amino Acid Sequence; D003094:Collagen / Q000378:metabolism; D003238:Connective Tissue / Q000648:ultrastructure; D046911:Macromolecular Substances; D008958:Models, Molecular; D013329:Structure-Activity Relationship
D046911:Macromolecular Substances; D003094:Collagen