Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Toxins (Basel). 2021 May 1;13(5):329. doi: 10.3390/toxins13050329.
A majority of toxins produced by type I toxin-antitoxin (TA-1) systems are small membrane-localized proteins that were initially proposed to kill cells by forming non-specific pores in the cytoplasmic membrane. The examination of the effects of numerous TA-1 systems indicates that this is not the mechanism of action of many of these proteins. produces two toxins of the Fst/Ldr family, one encoded on pheromone-responsive conjugative plasmids (Fst) and the other on the chromosome, Fst. Previous results demonstrated that overexpression of the toxins produced a differential transcriptomic response in cells. In this report, we identify the specific amino acid differences between the two toxins responsible for the differential response of a gene highly induced by Fst but not Fst. In addition, we demonstrate that a transporter protein that is genetically linked to the chromosomal version of the TA-1 system functions to limit the toxicity of the protein.
I 型毒素-抗毒素(TA-1)系统产生的大多数毒素是小的膜定位蛋白,最初被提议通过在细胞质膜中形成非特异性孔来杀死细胞。对许多 TA-1 系统的作用的研究表明,这不是许多这些蛋白质的作用机制。产生两种 Fst/Ldr 家族的毒素,一种编码在与激素反应的可接合质粒(Fst)上,另一种编码在染色体上,Fst。先前的结果表明,毒素的过表达导致 细胞中差异转录组响应。在本报告中,我们确定了两个毒素之间的特定氨基酸差异,这些差异负责由 Fst 但不是 Fst 高度诱导的基因的差异响应。此外,我们证明了与染色体 TA-1 系统的染色体版本基因连锁的转运蛋白在限制蛋白毒性方面起作用。