תפריט נגישות
ניגודיות עדינהניגודיות גבוהה
מונוכרום
הדגשת קישורים
חסימת אנימציה
פונט קריא
סגור
איפוס הגדרות נגישות
להורדת מודול נגישות חינם תפריט נגישותניגודיות עדינהניגודיות גבוההמונוכרוםהדגשת קישוריםחסימת אנימציהפונט קריאסגוראיפוס הגדרות נגישותלהורדת מודול נגישות חינםJanak Raj Joshi
Netaly Khazanov
Amy Charkowski
Adi Faigenboim
Hanoch Senderowitz
Iris Yedidia
In the battle between bacteria and plants, bacteria often use a population density-dependent regulatory system known as quorum sensing (QS) to coordinate virulence gene expression. In response, plants use innate and induced defense mechanisms that include low-molecular-weight compounds, some of which serve as antivirulence agents by interfering with the QS machinery. The best-characterized QS system is driven by the autoinducer N-acyl-homoserine lactone (AHL), which is produced by AHL synthases (LuxI homologs) and perceived by response regulators (LuxR homologs). Several plant compounds have been shown to directly inhibit LuxI or LuxR. Gaining atomic-level insight into their mode of action and how they interfere with QS enzymes supports the identification and design of novel QS inhibitors. Such information can be gained from molecular modeling and docking simulations. The summary of these interactions shows that plant-derived compounds act as interkingdom cues and that these allomones specifically target bacterial communication systems.
Janak Raj Joshi
Netaly Khazanov
Amy Charkowski
Adi Faigenboim
Hanoch Senderowitz
Iris Yedidia
In the battle between bacteria and plants, bacteria often use a population density-dependent regulatory system known as quorum sensing (QS) to coordinate virulence gene expression. In response, plants use innate and induced defense mechanisms that include low-molecular-weight compounds, some of which serve as antivirulence agents by interfering with the QS machinery. The best-characterized QS system is driven by the autoinducer N-acyl-homoserine lactone (AHL), which is produced by AHL synthases (LuxI homologs) and perceived by response regulators (LuxR homologs). Several plant compounds have been shown to directly inhibit LuxI or LuxR. Gaining atomic-level insight into their mode of action and how they interfere with QS enzymes supports the identification and design of novel QS inhibitors. Such information can be gained from molecular modeling and docking simulations. The summary of these interactions shows that plant-derived compounds act as interkingdom cues and that these allomones specifically target bacterial communication systems.
