Tit-for-Tat: Type VI Secretion System Counterattack during Bacterial Cell-Cell Interactions

نویسندگان

  • Marek Basler
  • Brian T. Ho
  • John J. Mekalanos
چکیده

The bacterial type VI secretion system (T6SS) is a dynamic organelle that bacteria use to target prey cells for inhibition via translocation of effector proteins. Time-lapse fluorescence microscopy has documented striking dynamics of opposed T6SS organelles in adjacent sister cells of Pseudomonas aeruginosa. Such cell-cell interactions have been termed "T6SS dueling" and likely reflect a biological process that is driven by T6SS antibacterial attack. Here, we show that T6SS dueling behavior strongly influences the ability of P. aeruginosa to prey upon heterologous bacterial species. We show that, in the case of P. aeruginosa, T6SS-dependent killing of either Vibrio cholerae or Acinetobacter baylyi is greatly stimulated by T6SS activity occurring in those prey species. Our data suggest that, in P. aeruginosa, T6SS organelle assembly and lethal counterattack are regulated by a signal that corresponds to the point of attack of the T6SS apparatus elaborated by a second aggressive T6SS(+) bacterial cell. PAPERFLICK:

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Gaming the competition in microbial cell-cell interactions.

It helps to pay attention to an opponent’s prior actions when playing strategy games, be they chess, poker or rock-paper-scissors. In a thought provoking paper by Basler et al (2013), published in Cell, we have a chance to watch bacteria ‘game’ each other in a deadly match of life or death involving the deployment of a potent weapon called the Type VI Secretion System (T6SS; Basler et al, 2013)...

متن کامل

Dual Role for DsbA in Attacking and Targeted Bacterial Cells during Type VI Secretion System-Mediated Competition

Incorporation of disulfide bonds into proteins can be critical for function or stability. In bacterial cells, the periplasmic enzyme DsbA is responsible for disulfide incorporation into many extra-cytoplasmic proteins. The type VI secretion system (T6SS) is a widely occurring nanomachine that delivers toxic effector proteins directly into rival bacterial cells, playing a key role in inter-bacte...

متن کامل

Molecular weaponry: diverse effectors delivered by the Type VI secretion system

The Type VI secretion system is a widespread bacterial nanomachine, used to deliver toxins directly into eukaryotic or prokaryotic target cells. These secreted toxins, or effectors, act on diverse cellular targets, and their action provides the attacking bacterial cell with a significant fitness advantage, either against rival bacteria or eukaryotic host organisms. In this review, we discuss th...

متن کامل

Type 6 secretion dynamics within and between bacterial cells.

The bacterial type 6 secretion system (T6SS) functions as a virulence factor capable of attacking both eukaryotic and prokaryotic target cells by a process that involves protein transport through a contractile bacteriophage tail-like structure. The T6SS apparatus is composed, in part, of an exterior sheath wrapped around an interior tube. Here, we report that in living cells the cytoplasmic ade...

متن کامل

The roles of EPIYA sequence to perturb the cellular signaling pathways and cancer risk

Abstract It was shown that several pathogenic bacterial effector proteins contain the Glu-Pro-Ile-Tyr-Ala (EPIYA) or a similar sequence. These bacterial EPIYA effectors are delivered into host cell via type III or IV secretion system, where they undergo tyrosine phosphorylation at the EPIYA sequences, which triggers interaction with multiple host cell SH2 domain-containing proteins and thereby...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cell

دوره 152  شماره 

صفحات  -

تاریخ انتشار 2013