Goodson Michael S, Crookes-Goodson Wendy J, Kimbell Jennifer R, McFall-Ngai Margaret J
Department of Medical Microbiology and Immunology, University of Wisconsin, Madison, Wisconsin 53706, USA.
Biol Bull. 2006 Aug;211(1):7-17. doi: 10.2307/4134573.
Within hours of hatching, the squid Euprymna scolopes forms a specific light organ symbiosis with the marine luminous bacterium Vibrio fischeri. Interactions with the symbiont result in the loss of a complex ciliated epithelium dedicated to promoting colonization of host tissue, and some or all of this loss is due to widespread, symbiont-induced apoptosis. Members of the p53 family, including p53, p63, and p73, are conserved across broad phyletic lines and p63 is thought to be the ancestral gene. These proteins have been shown to induce apoptosis and developmental morphogenesis. In this study, we characterized p63-like transcripts from mRNA isolated from the symbiotic tissues of E. scolopes and described their role in symbiont-induced morphogenesis. Using degenerate RT-PCR and RACE PCR, we identified two p63-like transcripts encoding proteins of 431 and 567 amino acids. These transcripts shared identical nucleotides where they overlapped, suggesting that they are splice variants of the same gene. Immunocytochemistry and Western blots using an antibody specific for E. scolopes suggested that the p53 family members are activated in cells of the symbiont-harvesting structures of the symbiotic light organ. We propose that once the symbiosis is initiated, a symbiont-induced signal activates p53 family members, inducing apoptosis and developmental morphogenesis of the light organ.
孵化后的数小时内,夏威夷短尾乌贼(Euprymna scolopes)便会与海洋发光细菌费氏弧菌(Vibrio fischeri)形成特定的发光器官共生关系。与共生体的相互作用导致一种专门促进宿主组织定殖的复杂纤毛上皮细胞丧失,这种丧失部分或全部归因于共生体诱导的广泛凋亡。p53家族成员,包括p53、p63和p73,在广泛的系统发育谱系中保守,并且p63被认为是祖先基因。这些蛋白质已被证明可诱导细胞凋亡和发育形态发生。在本研究中,我们对从夏威夷短尾乌贼共生组织分离的mRNA中的p63样转录本进行了表征,并描述了它们在共生体诱导的形态发生中的作用。使用简并RT-PCR和RACE PCR,我们鉴定出两个p63样转录本,分别编码431和567个氨基酸的蛋白质。这些转录本在重叠处共享相同的核苷酸,表明它们是同一基因的剪接变体。使用针对夏威夷短尾乌贼的特异性抗体进行免疫细胞化学和蛋白质印迹分析表明,p53家族成员在共生发光器官的共生体收集结构的细胞中被激活。我们提出,一旦共生开始,共生体诱导的信号会激活p53家族成员,诱导发光器官的细胞凋亡和发育形态发生。