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Example sentences for: filaments
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is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [ 8 ] . Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [ 9 10 11 ] . Control of thin filament length is critical for maintaining proper sarcomere function and length [ 12 ] . Inhibition of Tmod1's capping activity - either by using an antibody to its C-terminal end or by decreasing expression using an antisense Tmod1 transcript - results in elongated thin filaments and decreased cardiac contractility [ 13 14 ] . Tmod1 overexpression in rat cardiomyocytes causes shortening of the thin filaments and sarcomere disorganization, resulting in myofibril degeneration [ 14 ] . Likewise, mice overexpressing TMOD1 in the heart show disrupted sarcomere organization with shortened thin filaments, leading to myofibril degeneration and dilated cardiomyopathy [ 15 ] . Recently, Littlefield and colleagues showed that overexpression of GFP-Tmod1 in chick cardiac myocytes results in shortening of thin filaments; the authors proposed that excess Tmod1 decreases the affinity between actin monomers and pointed ends, leading to monomer dissociation and filament shortening [ 42 ] . Mutations in many proteins making up the cardiac sarcomere have been shown to cause cardiac hypertrophy [ 16 17 18 19 ] :mutations in the TPM1 gene, for example, cause type 3 familial hypertrophic cardiomyopathy (CMH3), and a transgenic mouse expressing a CMH3 mutation develops ventricular myocyte disarray and hypertrophy [ 20 ] . Mutations in myosin heavy chain 7 are estimated to account for 40-50% of the cases of hypertrophic cardiomyopathy [ 21 ] .
Myosin-II recruitment to the cortex and to the cleavage furrow cortex depends on the thick filament-state of this molecular motor [ 5 6 7 8 ] . The ability to form thick filaments is regulated by phosphorylation of three threonines near the tail of the long coiled-coil.
Again, it is quite possible that the microdomain-anchored short actin filaments, proposed above, may allow the docking and assembly of subviral particles inside the infected cell.
As cytochalasin D has a high affinity (50 nM) for the growing ends of actin filaments, this treatment should inhibit polymerization of existing filaments but should not block new filament formation [ 23 ] . Thus the actin incorporated most likely reflects nucleation of new filaments, as previously discussed [ 24 ] . As expected, cells treated with cytochalasin D during permeabilization showed no actin incorporation (data not shown).
19 μm [ 29 ] . Based upon these results, we suggest that GFP-MHCK-C may colocalize with myosin II thick filaments by binding at the bare zone.
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