| pubmed-article:7599033 | pubmed:abstractText | Like in other organisms tested to date, adapted cells of Lactococcus lactis subsp. lactis IL1403 pretreated at 42 degrees C for 30 min develop a thermotolerant state, i.e. an increased ability to survive subsequent exposure to a lethal challenge temperature (52 degrees C for 15 or 30 min). In different cellular systems, chemicals as diverse as divalent metal salts, natural or synthetic compounds trigger the development of thermotolerance. Yet, in L. lactis subsp. lactis IL1403, among the 17 chemicals tested, only four induced this transient increased tolerance to heat: cadmium chloride, mercury chloride, sodium azide and beta-mercaptoethanol. Intriguingly, none of these four compounds induced the synthesis of three major heat shock proteins (DnaK, GroEL and hsp104-analogue), which are believed to be responsible for thermotolerance in most organisms. It is suggested that: (i) the lesions produced by these various 'proteotoxic' agents are fundamentally different from those produced by heat; (ii) heat shock protein synthesis and transient induced tolerance to heat are not tightly correlated phenomena in L. lactis subsp. lactis as they are in Escherichia coli and some other organisms. | lld:pubmed |
