Sulfate restriction induces hyposecretion of the adhesion proteoglycan and cell hypomotility associated with increased 35SO42− uptake and expression of a band 3 like protein in the marine sponge, Microciona prolifera
Corresponding Author
William J. Kuhns
Hospital for Sick Children, Toronto, Canada M5G 1X8
Marine Biological Laboratory, Woods Hole, Massachusetts
Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, CanadaSearch for more papers by this authorOctavian Popescu
Institute for Biological Research, Cluj/Napoca, Romania
Search for more papers by this authorMax M. Burger
Friedrich Miescher Institute, University Hospital of Basel, Switzerland
Marine Biological Laboratory, Woods Hole, Massachusetts
Search for more papers by this authorGradimir Misevic
Department of Research, University Hospital of Basel, Switzerland
Marine Biological Laboratory, Woods Hole, Massachusetts
Search for more papers by this authorCorresponding Author
William J. Kuhns
Hospital for Sick Children, Toronto, Canada M5G 1X8
Marine Biological Laboratory, Woods Hole, Massachusetts
Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, CanadaSearch for more papers by this authorOctavian Popescu
Institute for Biological Research, Cluj/Napoca, Romania
Search for more papers by this authorMax M. Burger
Friedrich Miescher Institute, University Hospital of Basel, Switzerland
Marine Biological Laboratory, Woods Hole, Massachusetts
Search for more papers by this authorGradimir Misevic
Department of Research, University Hospital of Basel, Switzerland
Marine Biological Laboratory, Woods Hole, Massachusetts
Search for more papers by this authorAbstract
Sulfate is an important component relating to normal proteoglycan secretion and normal motility in the marine sponge, Microciona prolifera. The following alterations were observed in sponge cells when sulfate free artificial sea water was used as the suspension medium: (1) impairment of aggregation, (2) loss of cell movements, (3) a marked reduction in the secretion of the adhesion proteoglycan (AP). Reversal of this effect occurred if sulfate depleted cells were again rotated in sulfate containing artificial sea water. Motility and reaggregation of sulfate deprived cells could be completely restored by purified AP, but only if cells were first pre-conditioned in normal sea water. Comparisons of 35SO42− uptake between normal and sulfate deprived cells which had been treated to reduce preformed secretions showed a marked increase in 35SO42− uptake and incorporation which could be greatly augmented in the presence of Ca2+/Mg2+. Excessive retention of AP in sulfate starved cells demonstrated by immunostaining suggested that AP secretion and cellular motility may be controlled by a sulfate dependent secretogogue or that undersulfated AP itself had developed a secretory defect. SDS-PAGE of Triton treated cellular extracts demonstrated a 116 kDa 35SO42− sulfated band which co-migrated with AP, but only in extracts derived from sulfate starved cells. Western blots prepared from such extracts incubated in the presence of a monoclonal anti-band 3 antibody demonstrated labelling of a single 97 kDa band only in material from sulfate deprived cells. The absence of this component in normal cell extracts indicated that this protein may be involved in facilitated sulfate transport. This study lends support to a heretofore unrecognized role for sulfate in cell motility and secretion.
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