嗜酸嗜酸古细菌缺乏sigma因子和细菌基因组中广泛存在的大量热休克蛋白(HSP),建议涉及其他处理热应力的策略。嗜酸古细菌的热休克转录组(f。Sulfolobus)solfataricus98/2揭示了对热胁迫高度响应的基因,包括转录调节因子YtrAS(Ssol_2420)和FadRS(Ssol_0314),以及II型毒素-抗毒素(TA)基因座VapBC6(Ssol_2337,Ssol_2338)和VapBC22(Ssol_0819,Ssol_0818)。角色,如果有的话,在微生物应激反应过程中,II型TA基因座,如大肠杆菌,是有争议的。但是,当基因编码YtrASs时,FadRS,VapC22、VapB6和VapC6在Sa中进行了系统突变。solfataricus98/2,观察到该组内其他基因的显着上调,在热应力响应过程中暗示了一个相互连接的调节网络。VapBC6和VapBC22在其他硫磺属中具有密切的同源物,以及其他古细菌(例如,热球菌和古细菌),它们的相应基因也具有热休克反应性。Sasolfataricus98/2中VapBCTA基因座与热休克调节剂之间的相互作用不仅表明了与细菌不同的热休克反应的细胞机制,而且在嗜热古细菌中可能具有共同特征。
Thermoacidophilic archaea lack sigma factors and the large inventory of heat shock proteins (HSPs) widespread in bacterial genomes, suggesting other strategies for handling thermal stress are involved. Heat shock transcriptomes for the thermoacidophilic archaeon Saccharolobus (f. Sulfolobus) solfataricus 98/2 revealed genes that were highly responsive to thermal stress, including transcriptional regulators YtrASs (Ssol_2420) and FadRSs (Ssol_0314), as well as type II toxin-antitoxin (TA) loci VapBC6 (Ssol_2337, Ssol_2338) and VapBC22 (Ssol_0819, Ssol_0818). The role, if any, of type II TA loci during stress response in microorganisms, such as Escherichia coli, is controversial. But, when genes encoding YtrASs , FadRSs , VapC22, VapB6, and VapC6 were systematically mutated in Sa. solfataricus 98/2, significant up-regulation of the other genes within this set was observed, implicating an interconnected regulatory network during thermal stress response. VapBC6 and VapBC22 have close homologues in other Sulfolobales, as well as in other archaea (e.g. Pyrococcus furiosus and Archaeoglobus fulgidus), and their corresponding genes were also heat shock responsive. The interplay between VapBC TA loci and heat shock regulators in Sa solfataricus 98/2 not only indicates a cellular mechanism for heat shock response that differs from bacteria but one that could have common features within the thermophilic archaea.