Abstract

During normal chicken development tenascin begins to accumulate in the dermis of anterior metatarsal skin at the time of scutate scale ridge formation, and is localized in a distinct pattern along the outer scale surface. Anterior metatarsal skin from scaleless (sc/sc) embryos, which do not form scutate scales, begins to accumulate tenascin 4 days later than normal skin. This study shows that normal and scaleless anterior metatarsal dermis accumulate the same tenascin isoforms and undergo the same isoform changes in the post-hatch period, but there is less tenascin accumulated in scaleless dermis and there is no pattern to its distribution. In both normal and scaleless anterior metatarsal skin, tenascin mRNA is localized in the dermis and is distributed in the same way as the protein. Thus, scaleless skin is defective in the ability to accumulate appropriate amounts of tenascin and to maintain the tenascin in the patterned manner of normal. Recombinant skin cultures show that epidermal-dermal interactions are required for tenascin accumulation. The dermis specifies the way that tenascin is organized, but interaction with epidermis is required to maintain this organization. The epidermal role appears to be permissive because in heterotypic recombinants, neither scaleless anterior metatarsal epidermis nor normal footpad epidermis changes the way that tenascin appears in the normal anterior metatarsal dermis; and in reciprocal recombinants, normal anterior metatarsal epidermis does not change the way tenascin is accumulated in either scaleless anterior metatarsal dermis or normal footpad dermis.

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