Rickettsia actin-based motility occurs in distinct phases mediated by different actin nucleators.
Rickettsia actin-based motility occurs in distinct phases mediated by different actin nucleators.
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DOI:
10.1016/j.cub.2013.11.025
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发表时间:
2014-01-06
期刊:
影响因子:
9.2
通讯作者:
Welch, Matthew D.
中科院分区:
文献类型:
--
作者:
Reed, Shawna C. O.;Lamason, Rebecca L.;Risca, Viviana I.;Abernathy, Emma;Welch, Matthew D.
Many intracellular bacterial pathogens undergo actin-based motility to promote cell-cell spread during infection. For each pathogen, motility was assumed to be driven by a single actin polymerization pathway. Curiously, spotted-fever-group Rickettsia differ from other pathogens in possessing two actin polymerizing proteins. RickA, an activator of the host Arp2/3 complex, was initially proposed to drive motility. Sca2, a mimic of host formins, was later shown to be required for motility. Whether and how their activities are coordinated has remained unclear. Here, we show that each protein directs an independent mode of Rickettsia parkeri motility at different times during infection. Early after invasion, motility is slow and meandering, generating short, curved actin tails that are enriched with Arp2/3 complex and cofilin. Early motility requires RickA and Arp2/3 complex, and is correlated with transient RickA localization to the bacterial pole. Later in infection, motility is faster and directionally persistent, resulting in long, straight actin tails. Late motility is independent of Arp2/3 complex and RickA, and requires Sca2, which accumulates at the bacterial pole. Both motility pathways facilitate cell-to-cell spread. The ability to exploit two actin assembly pathways may allow Rickettsia to establish an intracellular niche and spread between diverse cells throughout a prolonged infection.
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