MUMBAI, India, Sept. 28 -- Intellectual Property India has published a patent application (202511019534 A) filed by Gautam Buddha University on March 05, 2025, for Novel Ccdb Toxin From Xenorhabdus Nematophila.
Inventors include Dr. Jitendra Singh Rathore; Shobhi Chaudhary; and Garima Singh.
The application for the patent was published on September 25, 2026, under issue no. 39/2026.
Abstract: The present invention shows the discovery and characterization of ccdAB type II toxinantitoxin module from the entomopathogenic bacterium X nematophila. The module consists of 306 bp cedE toxin gene, and a 279 bp ccdA antitoxin gene. The discovery includes the heterologous gene expression of the cedE toxin in Escherichia coli which induces bacterial growth inhibition, however, the toxicity is neutralized in the presence of ccdA antitoxin. Since, the C-terminal region of CcdB toxin is believed to be important in the growth inhibition through interaction with DNA gyrase, a deletion construct was generated by deleting the C-terminal amino acids from 99 to I 0 I which showed growth recovery in E. coli. The site directed mutations of important residues mostly at C terminal responsible for CcdB toxicity, resulted in loss of its toxic effects in Escherichia coli. Further, a 305 bp region upstream of the ccdAE genes was identified as a promoter, and promoter-LacZ construct was constructed. Promoter activity was enhanced under various stress conditions, such as temperature changes, antibiotic exposure, and nutrient deprivation. The present invention also discloses autoregulation of ccdAB operon, as the ccdAE promoter activity is inhibited by the ccdA antitoxin, both independently as well as when combined with the cedE toxin. The autoregulatory mechanism was confirmed using Electrophoretic Mobility Shift Assay (EMSA), indicating that the CcdA antitoxin alone and CcdAB protein complex binds directly to its own promoter region. Gene expression was significantly increased in response to stress, particularly under SOS- inducing conditions, highlighting the ccdAE system as a tightly regulated and stress-responsive mechanism critical for bacterial survival.
Disclaimer: Curated by HT Syndication.
