Chicken lactose lectin: Cell-to-cell or cell-to-matrix adhesion molecule?

Abstract

Endogenous chicken muscle lectin isolated by lactose affinity chromatography inhibits myoblast fusion. Similar lectins isolated from embryonic brain, heart, and liver and from adult intestine exhibit the same ability. Elevated levels of any of these lectins canceled the inhibitory effect. Peanut agglutinin isolated by the same procedure had no effect at any concentration tested. Concanavalin A affected fusion only at high concentrations. Muscle lectin was shown to agglutinate myoblasts in microtiter plates, whereas exogenous addition in culture inhibited alignment as seen by time lapse microcinematography. Cell-to-cell communication between lectin-treated cells was shown by nucleotide exchange, and lectin-coated culture dishes did not affect cell attachment. Our evidence shows a lack of specificity to muscle, but suggests an aggregating capacity between cells, or possibly an interaction between the cell membrane and the extracellular matrix.

Endogenous muscle lectin inhibits myoblast adhesion to laminin.

“…Evidence for a role of L-14 in muscle fusion was first obtained more than a decade ago (Gartner and Podleski, 1976) at a time when cell-matrix interactions were poorly understood and laminin itself had not yet been discovered. Inhibition of muscle fusion by L-14 was confirmed in succeeding studies (Knudsen and Horowitz, 1978;MacBride and Przybylski, 1980;MacBride and Przybylski, 1986), but a range of evidence has been presented which argues against direct participation of L-14 in the fusion process (Den et al, 1976;Den and Chin, 1981;Kaufman and Lawless, 1980) . Instead, our results suggest that effects of L-14 on fusion might be indirectly a result of altered cell adhesion to laminin .…”

“…For use in cell culture, recombinant L-14 was alkylated with iodoacetamide (Whitney et al ., 1986) to stabilize the lectin against oxidative inactivation of its carbohydratebinding activity. Otherwise, L-14 is reported to be inactivated within 30 min in the oxidizing environment of tissue culture medium (MacBride and Przybylski, 1986 ;Whitney et al ., 1986) . The possibility is discussed below that extracellular oxidation might function biologically to limit the duration ofactivity ofsecreted L-14.…”