Shaw J M, Wellington J E, Walker G J
Institute of Dental Research, United Dental Hospital, Sydney, Australia.
Caries Res. 1997;31(6):441-50. doi: 10.1159/000262436.
A low molecular weight dextranase inhibitor from Streptococcus sobrinus has previously been identified and purified. The range of conditions under which inhibition occurs, and the situations in which dextranase activity of S. sobrinus can reappear, have been examined in the chemostat. These studies have revealed that when dextranase production exceeds that of the inhibitor, all the inhibitor is tightly bound into enzyme-inhibitor complexes, and the excess enzyme remains active. Another factor that influences the activity of dextranase inhibitor has now been identified, namely the ability of the inhibitor to bind to water-insoluble glucans. Adsorption to water-insoluble alpha-D-glucans, produced by oral streptococci that were grown in batch culture, increased with their proportion of alpha-1,3-linked sequences of glucose residues. Studies with water-insoluble dextrans of Leuconostoc mesenteroides strains showed that alpha-1,6-linked sequences were also important for binding. The inhibitor was not active when adsorbed to glucan, but active inhibitor was released by incubation with soluble dextran. The interactions of sucrose, alpha-D-glucosyltransferases, alpha-D-glucans, dextranase and dextranase inhibitor are discussed in relation to the growth rate of S. sobrinus. At low growth rate in the chemostat the predominant alpha-D-glucosyltransferase (GTF) is a GTF-S that converts sucrose into soluble dextran, and the activity of free dextranase inhibitor in the culture filtrate is high. By contrast, at high growth rate the streptococci produce GTFs capable of synthesizing water-insoluble alpha-D-glucans, and no free inhibitor is found in culture filtrate. Thus the activity of free, extracellular dextranase inhibitor is controlled by (i) the extent of binding to dextranase and (ii) the extent of adsorption to water-insoluble alpha-D-glucan.
先前已从嗜热栖热放线菌中鉴定并纯化出一种低分子量葡聚糖酶抑制剂。已在恒化器中研究了发生抑制作用的条件范围以及嗜热栖热放线菌葡聚糖酶活性重新出现的情况。这些研究表明，当葡聚糖酶的产生量超过抑制剂的产生量时，所有抑制剂都会紧密结合形成酶 - 抑制剂复合物，而过量的酶仍保持活性。现在已确定另一个影响葡聚糖酶抑制剂活性的因素，即抑制剂与水不溶性葡聚糖结合的能力。对分批培养的口腔链球菌产生的水不溶性α - D - 葡聚糖的吸附作用，随着其葡萄糖残基α - 1,3 - 连接序列比例的增加而增强。对肠膜明串珠菌菌株的水不溶性葡聚糖的研究表明，α - 1,6 - 连接序列对结合也很重要。抑制剂吸附到葡聚糖上时无活性，但与可溶性葡聚糖一起孵育可释放出活性抑制剂。结合嗜热栖热放线菌的生长速率，讨论了蔗糖、α - D - 葡萄糖基转移酶、α - D - 葡聚糖、葡聚糖酶和葡聚糖酶抑制剂之间的相互作用。在恒化器中生长速率较低时，主要的α - D - 葡萄糖基转移酶（GTF）是GTF - S，它将蔗糖转化为可溶性葡聚糖，培养滤液中游离葡聚糖酶抑制剂的活性较高。相比之下，在高生长速率时，链球菌产生能够合成水不溶性α - D - 葡聚糖的GTF，培养滤液中未发现游离抑制剂。因此，游离的细胞外葡聚糖酶抑制剂的活性受（i）与葡聚糖酶的结合程度和（ii）对水不溶性α - D - 葡聚糖的吸附程度控制。
