A novel protein Jpk induces bacterial cell death through reactive oxygen species.
Jpk, a trans-acting regulatory factor associating with the position-specific regulatory element of Hoxa-7, has been reported to induce cell death in both prokaryotic and eukaryotic cells upon overexpression. The N- and C-terminal deleted variants of Jpk were constructed and then the toxicity of each construct was analyzed by checking the viability of the cells and the concomitant morphological changes through electron microscopy following the expression. The N-terminus of Jpk harboring transmembrane domain seemed to be more toxic to bacterial cell than C-terminus and the morphology of bacterial cells expressing N-terminal Jpk was similar to that induced by full length Jpk. The toxicity caused by Jpk protein in bacterial cell was through the production of ROS, which was decreased by an antioxidant (DTT) in a concentration dependent manner. The finding described in this study provides valuable clues on the relationship between Jpk toxicity and ROS generation.
Department of Anatomy, Embryology Lab, BK 21 Project for Med. Sci., Yonsei University College of Medicine, Seoul, Republic of Korea. sdpark09@korea.kr
Sungdo
S
Park
Kyoung-Ah
KA
Kong
Myoung Hee
MH
Kim
D001426:Bacterial Proteins / Q000502:physiology*; D015153:Blotting, Western; D016923:Cell Death / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism*
D001426:Bacterial Proteins; D017382:Reactive Oxygen Species