The Small GTPase Rif Is Dispensable for Platelet Filopodia Generation in Mice

Robert Goggs, Joshua S. Savage, Harry Mellor, Alastair W. Poole

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


Background: Formation of filopodia and other shape change events are vital for platelet hemostatic function. The mechanisms regulating filopodia formation by platelets are incompletely understood however. In particular the small GTPase responsible for initiating filopodia formation by platelets remains elusive. The canonical pathway involving Cdc42 is not essential for filopodia formation in mouse platelets. The small GTPase Rif (RhoF) provides an alternative route to filopodia generation in other cell types and is expressed in both human and mouse platelets. Hypothesis/Objective: We hypothesized that Rif might be responsible for generating filopodia by platelets and generated a novel knockout mouse model to investigate the functional role of Rif in platelets. Methodology/Principal Findings: Constitutive RhoF-/- mice are viable and have normal platelet, leukocyte and erythrocyte counts and indices. RhoF-/- platelets form filopodia and spread normally on various agonist surfaces in static conditions and under arterial shear. In addition, RhoF-/- platelets have normal actin dynamics, are able to activate and aggregate normally and secrete from alpha and dense granules in response to collagen related peptide and thrombin stimulation. Conclusions: The small GTPase Rif does not appear to be critical for platelet function in mice. Functional overlap between Rif and other small GTPases may be responsible for the non-essential role of Rif in platelets.

Original languageEnglish
Article numbere54663
JournalPLoS ONE
Issue number1
Publication statusPublished - 30 Jan 2013

ASJC Scopus subject areas

  • General Biochemistry,Genetics and Molecular Biology
  • General Agricultural and Biological Sciences


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