Vilchèze Catherine, Molle Virginie, Carrère-Kremer Séverine, Leiba Jade, Mourey Lionel, Shenai Shubhada, Baronian Grégory, Tufariello Joann, Hartman Travis, Veyron-Churlet Romain, Trivelli Xavier, Tiwari Sangeeta, Weinrick Brian, Alland David, Guérardel Yann, Jacobs William R, Kremer Laurent
Howard Hughes Medical Institute, Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, New York, United States of America.
Laboratoire de Dynamique des Interactions Membranaires Normales et Pathologiques, Universités de Montpellier II et I, CNRS; UMR 5235, Montpellier, France.
PLoS Pathog. 2014 May 8;10(5):e1004115. doi: 10.1371/journal.ppat.1004115. eCollection 2014 May.
Mycobacterium tuberculosis bacilli display two signature features: acid-fast staining and the capacity to induce long-term latent infections in humans. However, the mechanisms governing these two important processes remain largely unknown. Ser/Thr phosphorylation has recently emerged as an important regulatory mechanism allowing mycobacteria to adapt their cell wall structure/composition in response to their environment. Herein, we evaluated whether phosphorylation of KasB, a crucial mycolic acid biosynthetic enzyme, could modulate acid-fast staining and virulence. Tandem mass spectrometry and site-directed mutagenesis revealed that phosphorylation of KasB occurred at Thr334 and Thr336 both in vitro and in mycobacteria. Isogenic strains of M. tuberculosis with either a deletion of the kasB gene or a kasB_T334D/T336D allele, mimicking constitutive phosphorylation of KasB, were constructed by specialized linkage transduction. Biochemical and structural analyses comparing these mutants to the parental strain revealed that both mutant strains had mycolic acids that were shortened by 4-6 carbon atoms and lacked trans-cyclopropanation. Together, these results suggested that in M. tuberculosis, phosphorylation profoundly decreases the condensing activity of KasB. Structural/modeling analyses reveal that Thr334 and Thr336 are located in the vicinity of the catalytic triad, which indicates that phosphorylation of these amino acids would result in loss of enzyme activity. Importantly, the kasB_T334D/T336D phosphomimetic and deletion alleles, in contrast to the kasB_T334A/T336A phosphoablative allele, completely lost acid-fast staining. Moreover, assessing the virulence of these strains indicated that the KasB phosphomimetic mutant was attenuated in both immunodeficient and immunocompetent mice following aerosol infection. This attenuation was characterized by the absence of lung pathology. Overall, these results highlight for the first time the role of Ser/Thr kinase-dependent KasB phosphorylation in regulating the later stages of mycolic acid elongation, with important consequences in terms of acid-fast staining and pathogenicity.
抗酸染色以及在人类中诱导长期潜伏感染的能力。然而,控制这两个重要过程的机制在很大程度上仍然未知。丝氨酸/苏氨酸磷酸化最近已成为一种重要的调节机制,使分枝杆菌能够根据其环境调整其细胞壁结构/组成。在此,我们评估了至关重要的分枝菌酸生物合成酶KasB的磷酸化是否能调节抗酸染色和毒力。串联质谱和定点诱变表明,KasB的磷酸化在体外和分枝杆菌中均发生在苏氨酸334和苏氨酸336处。通过专门的连锁转导构建了结核分枝杆菌的同基因菌株,这些菌株要么缺失kasB基因,要么缺失kasB_T334D/T336D等位基因,后者模拟KasB的组成型磷酸化。将这些突变体与亲本菌株进行生化和结构分析,结果表明两个突变菌株的分枝菌酸都缩短了4至6个碳原子,并且缺乏反式环丙烷化。总之,这些结果表明在结核分枝杆菌中,磷酸化会显著降低KasB的缩合活性。结构/建模分析表明,苏氨酸334和苏氨酸336位于催化三联体附近,这表明这些氨基酸的磷酸化会导致酶活性丧失。重要的是,与kasB_T334A/T336A磷酸化缺失等位基因相比,kasB_T334D/T336D磷酸模拟和缺失等位基因完全丧失了抗酸染色能力。此外,评估这些菌株的毒力表明,在气溶胶感染后,KasB磷酸模拟突变体在免疫缺陷和免疫健全的小鼠中均减弱。这种减弱的特征是没有肺部病理变化。总体而言,这些结果首次突出了丝氨酸/苏氨酸激酶依赖性KasB磷酸化在调节分枝菌酸延伸后期阶段的作用,在抗酸染色和致病性方面具有重要影响。