Actin Motor proteins

-hydrolyze ATP

-Cause sliding of Actin filaments

or

-movement of cargo along actin

conventional: form thick filaments

Unconventional myosin: do not form filaments, act as motors

• involved in actin/myosin sliding
• highly expressed in muscle cells
  • also found in non-muscle = forms part of contractile apparatus in cytokinesis
• 
  

• do not form filaments/ not involved in muscle contraction
• can be 1 or 2 headed molecules
• variety of cell movements
  • transport of membrane vesicles along actin
  • phagocytosis
  • extension of cell processes
    

1. N-terminal head domain(s): bind actin and exhibit ATPase activty 
2. Variable tail size, dictate specific interaction of myosin w/other proteins
3. some type of associated light chain
   

-central bare zone (just tails) is free of myosin heads

-myosin molecules (300) aggregate together (tail regions)

-thick filaments = bipolar

-->non muscle, smooth cells: myosin II filaments are much smaller (15-20 molecules)

• skeletal muscle: largest; muscle fibers
  • multinucleated cell
  • striated: orderly array of conctractile units
  • voluntary movements
  • form via fusion of myoblasts; once fused = nonmitotic
• Heart: resemble muscle fibers; also striated.
  
  • only have 1 nucleus per cell
• Smooth Muscle: no striations; found in regions like digestive track
• Myoepithelial: no striations; found in epithelia.
  
  • ectoderm derived
  • serve to expel fluids (saliva sweat, milk) from glandular tissues
    

cytoplasm comprised of microfibrils>sarcomeres>actin/myosin II

Z discs: attachment sites for + ends of actin filaments

A Band: "dark band", location of thick filaments

I band: "light bands" comprised of actin filaments.

• Titin: extend from Z disc to M line; associated w/myosin thick filament. Elastic and changes length as sarcomere contracts/relaxes

• Nebulin: same length as thin filaments;
  
• cap z: anchors + end of actin filament at Z discs
• actinin:
  

• Myosin II heads walk toward + ends of actin
  • Bringing thin filaments toward center
• Binding of ATP, releases myosin head from thin filament
• Release of phosphate = tight binding
  • force generating movement (power stroke)
• detached head: ATP hydrolyzed, cocks lever arm back to pre-stroke state
• ADP + P = weak affinity
  

Troponin-Tropomyosin Complex

(regulatory proteins)

• Tropomyosin = elongated molecule; binds along groove of actin helix
• Troponin = complex of 3 polypeptides
  
  • T-->
  • I--->bound to actin; inhibiting myosin-actin interaction
    
  • C-->binds calcium; causes I to release actin
    

-frequent cause of sudden death in young athletes

-inherited; heart enlargement and cardiac rhythm disturbances.

-linked to 40+ point mutations in genes coding for cadiac myosin heavy chains

-cardiac myosin PM-->greatly enlarged atria

-Dense bodies contain actinin; attach thin filaments to cell membrane

-intracellular scaffolding of intermediate (desmin) filaments

• smaller tail domains
• associate w/membrane vesicles organellesmyo
• myosin 1 = 1 headed motor

• in Microvilli
• may move membrane moelcules along core of actin bundles
• Myosin V (dimer) towards plus ends of actin
  

Intermediate Filaments

• Major structural elements; provide mechanical support and structure

• long lived, very stable; slow turnover

• not involved in cell motility

• abundant in cells

-highly conserved region = central rod domain

-rod domains of IF form dimeric coiled-coils

-tetramers formed by anti-parallel aggregation of 2 coiled-coil dimers

-tetramers aggregate end to end -->protofilaments

-Present intracellularly in skin

--->desmosmes, hemidesmosomes

->present extracellularly

---->kertanized layer of skin

->special derivatives of epithelial cells (hair and nails)

-autosomal dominant disease

-mutations of Keratin genes that affect deeper layers of epidermis (basal skin layer)

-Mild mechanical stresses-->rupture of basal cells, sloughing off of skin, blistering

-found in mature astrocytes

-expression increases in reactive astrocytes and forms "cellular scar" after injuries to CNS

-after CNS injury, astrocytic processes hypertrophy-->by addition of GFAP filaments

-marker for brain tumors

-form the nuclear lamina

-filaments that line inner face of nuclear envelope

-have longer central rod domain than other IF proteins

-nuclear import signal

-form sheetlike lattice

-regulated by phosphorylation/deP events synchronized to events of mitosis