Journal
CELLULAR MICROBIOLOGY
Volume 21, Issue 10, Pages -Publisher
WILEY
DOI: 10.1111/cmi.13076
Keywords
apoptosis; DNA damage response; IQS; POT1; Pseudomonas aeruginosa
Categories
Funding
- National Natural Research Foundation of China [31330002]
- Guangdong Technological Innovation Strategy of Special Funds [2018B020205003]
- National Program on Key Basic Research Project (973 Program) of China [2015CB150600]
- Guangzhou Science and Technology Key Project [201804020066]
- IMCB, the Agency of Science, Technology and Research (A*STAR)
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Pseudomonas aeruginosa, an opportunistic life-threatening human bacterial pathogen, employs quorum-sensing (QS) signal molecules to modulate virulence gene expression. 2-(2-hydroxyphenyl)-thiazole-4-carbaldehyde (IQS) is a recently identified QS signal that integrates the canonical lasR-type QS of P. aeruginosa and host phosphate stress response to fine-tune its virulence production for a successful infection. To address the role of IQS in pathogen-host interaction, we here present that IQS inhibits host cell growth and stimulates apoptosis in a dosage-dependent manner. By downregulating the telomere-protecting protein POT1 in host cells, IQS activates CHK1, CHK2, and p53 in an Ataxia telangiectasia mutated (ATM)/ATM and RAD3-related (ATR)-dependent manner and induces DNA damage response. Overexpression of POT1 in host cells presents a resistance to IQS treatment. These results suggest a pivotal role of IQS in host apoptosis, highlighting the complexity of pathogenesis mechanisms developed by P. aeruginosa during infection.
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