College of Pharmacy, Chonnam National University, Gwangju, Republic of Korea.
PLoS One. 2024 Aug 2;19(8):e0307512. doi: 10.1371/journal.pone.0307512. eCollection 2024.
The multifunctional autoprocessing repeat-in-toxin (MARTX) toxin is the primary virulence factor of Vibrio vulnificus displaying cytotoxic and hemolytic properties. The cysteine protease domain (CPD) is responsible for activating the MARTX toxin by cleaving the toxin precursor and releasing the mature toxin fragments. To investigate the structural determinants for inositol hexakisphosphate (InsP6)-mediated activation of the CPD, we determined the crystal structures of unprocessed and β-flap truncated MARTX CPDs of Vibrio vulnificus strain MO6-24/O in complex with InsP6 at 1.3 and 2.2Å resolution, respectively. The CPD displays a conserved domain with a central seven-stranded β-sheet flanked by three α-helices. The scissile bond Leu3587-Ala3588 is bound in the catalytic site of the InsP6-loaded form of the Cys3727Ala mutant. InsP6 interacts with the conserved basic cleft and the β-flap inducing the active conformation of catalytic residues. The β-flap of the post-CPD is flexible in the InsP6-unbound state. The structure of the CPD Δβ-flap showed an inactive conformation of the catalytic residues due to the absence of interaction between the active site and the β-flap. This study confirms the InsP6-mediated activation of the MARTX CPDs in which InsP6-binding induces conformational changes of the catalytic residues and the β-flap that holds the N terminus of the CPD in the active site, facilitating hydrolysis of the scissile bond.
多功能自加工重复入毒素(MARTX)毒素是创伤弧菌的主要毒力因子,具有细胞毒性和溶血特性。半胱氨酸蛋白酶结构域(CPD)通过切割毒素前体并释放成熟毒素片段,负责激活 MARTX 毒素。为了研究肌醇六磷酸(InsP6)介导的 CPD 激活的结构决定因素,我们分别以 1.3 和 2.2Å 的分辨率测定了未加工和β-折迭缺失的创伤弧菌 MO6-24/O 株 MARTX CPD 与 InsP6 复合物的晶体结构。CPD 显示出一个保守的结构域,其中央有一个七股β-折叠,两侧有三个α-螺旋。切割键 Leu3587-Ala3588 结合在 Cys3727Ala 突变体中 InsP6 负载形式的催化位点。InsP6 与保守的碱性裂缝和β-折迭相互作用,诱导催化残基的活性构象。CPD 后β-折迭在 InsP6 非结合状态下具有柔性。CPD Δβ-折迭的结构显示出催化残基的无活性构象,这是由于活性位点和β-折迭之间缺乏相互作用。这项研究证实了 InsP6 介导的 MARTX CPDs 的激活,其中 InsP6 结合诱导催化残基和β-折迭的构象变化,将 CPD 的 N 端保持在活性位点,促进了切割键的水解。