Biomedical Engineering Reference
In-Depth Information
We have seen how actomyosin contractility influences the stability of the SFs,
which are known to modulate focal adhesion dynamics, as previously reported
(Verkhovsky et al.
1999
; Hayakawa et al.
2005
; Costa et al.
2002
). In fact, the
contraction of SFs has been shown to result in the retraction of the cell rear edge,
dynamics of focal adhesions and translocation of the cell body (Choquet et al.
1997
;
Kaverina et al.
2002
; Tan et al.
2003
), (Small et al.
1996
; Lee et al.
1993
; Anderson
and Cross
2000
), (Anderson et al.
1996
; Verkhovsky et al.
1997
,
1999
).
In addition, contractile forces in the actin filament network causes network con-
traction in the lamellipodia and the cell body region (Verkhovsky et al.
1999
;
Svitkina et al.
1997
), resulting in the generation of retrograde and anterograde flows
(Vallotton et al.
2004
,
2005
; Schaub et al.
2007
). The two opposing flows finally
merge at the convergence zone, resulting in increased network compression
(Vallotton et al.
2004
).
Furthermore, as suggested by the selective depolymerization model discussed
in Chap.
4
, negative strain contributes to the depolymerization of actin filaments
by coupling with other biochemical factors such as ADF/Cofilin (Adachi et al.
2009
). Depolymerization, in turn, provides new monomers for continued polym-
erization (Pollard and Borisy
2003
; Mitchison and Cramer
1996
), which leads to
protrusion.
Meanwhile, the newly formed actin filaments are transported by retrograde flow
toward the back of the lamellipodia (Verkhovsky et al.
1999
; Henson et al.
1999
),
where they undergo realignment before they are incorporated into new fiber bun-
dles, facilitated by actomyosin tension (Kolega
2006
; Verkhovsky et al.
1995
). The
newly formed bundles then resume the role of tension generation, and the cycle is
repeated. Thus, the actin cytoskeletal structure can be regarded as a spatiotempo-
rally self-regulating mechanical system.
In summary, we have highlighted the roles played by actomyosin contractility in
driving F-actin network flow and deformation. We have not elaborated on the known
roles of the actomyosin system, which functions as the mechanical force generator.
We have also tried to put it into perspective the involvement of mechanical factors
such as strain in the self-regulatory mechanism of the actin cytoskeletal structure.
We believe that by considering the proposed mechanism alongside other known
molecular pathways (Pollard and Borisy
2003
), we can achieve a better understanding
of the underlying mechanisms of cell motility.
5.8
Conclusion
In this chapter, we have carried out quantitative analysis of the influence of actomy-
sosin contractility on actin network dynamics. We looked at the effect of perturbing
actomyosin contractility on both F-actin network flow and network deformation.
We have shown that flow fields of F-actin network in the lamellipodia of
actively migrating fish keratocytes are characterized by retrograde flow at the
front and anterograde flow at the back of the lamellipodia, and that the two flows
merge to form a convergence zone of reduced flow intensity. This is consistent
