Biochemistry of Metabolism: Cell Biology Microtubules Copyright © 2000-2006 by Joyce J. Diwan. All rights reserved. An a,b-tubulin heterodimer is the basic structural unit of microtubules. ab GTP GTP The heterodimer does not come apart, once formed. tubulin heterodimer The a & b tubulins, each about 55 kDa, are homologous but not identical. Each has a nucleotide binding site. a-Tubulin has a bound GTP, that does not hydrolyze. b-Tubulin may have bound GTP or GDP. Under certain conditions, b-tubulin can hydrolyze its bound GTP to GDP plus Pi, release Pi, and exchange the GDP for GTP. A microtubule is a hollow cylinder, about 24 nm in diameter. b-GTP a-GTP + Along the microtubule axis, tubulin heterodimers join end-to-end to form protofilaments, with alternating a & b subunits. b-GDP a-GTP Staggered assembly of 13 seam protofilaments yields a helical arrangement of tubulin microtubule 3-start helix heterodimers in the cylinder wall. Website with an image of a 3-D reconstruction of the structure of an intact microtubule, based on cryo-EM and image processing (by the Visualization Group at Lawrence Berkeley National Laboratory, K. Downing's research group). b-GTP a-GTP Electron microscopy of microtubules decorated with motor protein heads indicate a "3-start helix.“ Each turn of the helix spans 3 tubulin monomers (e.g., a, b, a). b-GDP a-GTP + seam microtubule 3-start helix This results in the wall having a "seam" where, instead of the predominant aa & bb lateral contacts, a subunits are laterally adjacent to b. During in vitro microtubule assembly, heterodimers join endto-end to form protofilaments. b-GTP a-GTP + These associate laterally to form sheets, & eventually microtubules. Heterodimers can add or dissociate at either end of a microtubule in vitro, but there is greater tendency for subunits to add at the plus end, where b-tubulin is exposed. b-GDP a-GTP seam microtubule 3-start helix As with actin filaments, microtubules can undergo treadmilling, with: • addition of tubulin heterodimers at the plus end • dissociation of tubulin heterodimers at the minus end. abab GTP GDP GTP GTP () protofilament (+) GTP must be bound to both a & b subunits for a tubulin heterodimer to associate with other heterodimers to form a protofilament or microtubule. Subunit addition brings b-tubulin that was exposed at the plus end into contact with a-tubulin. This promotes hydrolysis of GTP bound to the now interior b-tubulin. Pi dissociates, but b-tubulin within a microtubule cannot exchange its bound GDP for GTP. The GTP on a-tubulin does not hydrolyze. abab GTP GDP GTP GTP () protofilament (+) The minus end of a-tubulin may contribute an essential residue to the catalytic site of b-tubulin. Thus the minus end of an a subunit may serve as GAP (GTPase activating protein) for b-tubulin of the adjacent dimer in a protofilament. A homologous bacterial protein FtsZ is considered the ancestor of tubulin. FtsZ, which has a role in bacterial cytokinesis, also assembles into protofilaments, and the FtsZ protofilaments can associate to form sheets or tubules. abab GTP GDP GTP GTP () protofilament (+) Protofilament structure has been determined at atomic resolution using cryo-EM (electron diffraction) analysis of 2-D crystals induced by treating tubulin with zinc ions in the presence of a derivative of the drug taxol. These “zinc sheets” consist of parallel arrays of protofilaments. tubulin a,b dimer taxol GTP minus end GDP plus end a b PDB 1JFF Each nucleotide in the protofilament is at an a-b interface. The inability of GTP to dissociate from the a-subunit is consistent with occlusion by a loop from the b-subunit. A similar occlusion would account for the inability of b-tubulin within a protofilament to exchange GDP/GTP. GDP The nucleotide binds adjacent to a b-sheet (in magenta). The nucleotide binding site of tubulins is structurally similar to the nucleotide binding site of GTP-binding proteins b-tubulin of the Ras superfamily. PDB 1JFF Nucleotide binding sites of the motor proteins myosin and kinesin (to be discussed later) are also structurally similar to that of Ras. GDP b-tubulin PDB 1JFF The nucleotide-binding domain of tubulins includes a highly conserved sequence GGGTG(T/S)G, shown in black, that is part of a loop & helix that extends from one of the b-strands & passes near the nucleotide phosphates. View an animation depicting assembly of microtubules. Then explore the structure of the a,b-tubulin heterodimer, using Chime. A B A B C Doublet & triplet microtubules: The wall of one microtubule partly consists of the wall of an attached microtubule. The A tubule is a complete microtubule cylinder, made of 13 protofilaments. “Piggyback” B or C tubules are made of less than 13 protofilaments, usually 10. Centrioles are cylindrical structures, usually found in pairs orientated at right angles to one another. The wall of each centriole cylinder is made of nine interconnected triplet microtubules, arranged as a pinwheel. Centrioles at right angles, as in the centrosome. cartwheel structure at one end The interior of each centriole appears empty, except for a "cartwheel" structure at one end. Electron micrographs show appendages that protrude from the outer surface at one end of a mature centriole, & fibrous structures connecting the two centriole cylinders. Centriolar microtubules are relatively stable. The a,b tubulin heterodimers present in centriolar triplet microtubules are modified by polyglutamylation. Additional tubulins d,e,z,&h, as well as other proteins, are either present in centrioles or required for their formation. Centrioles at right angles, as in the centrosome. cartwheel structure at one end There is some variability in composition among different organisms. Basal bodies of cilia & flagella are also centrioles. Electron micrograph in article by J. Beisson & M. Wright. Centriole cylinders separate. (Biogenesis of ciliary basal bodies, which is somewhat different, will not be discussed here.) Shorter cylinders of same diameter appear at right angles & lengthen. During centriole duplication prior to mitosis (G1-S phase): The 2 centriole cylinders separate. A daughter centriole grows from a short disk-like structure at right angles to each parent centriole. A line through each daughter centriole bisects the parent. Centrioles at right angles, as in the centrosome. cartwheel structure at one end The centrosome, a mass of protein also called the microtubule organizing center (MTOC) or pericentriolar material, surrounds centrioles in animal cells. Following duplication, the pericentriolar material initially is associated only with each parent centriole cylinder. Centrioles at right angles, as in the centrosome. Proteins present in the pericentriolar material or on the surface of centrioles include centrin, pericentrin, ninein, cenexin, CEP110, CEP250 (C-Nap1), g-tubulin, and others. cartwheel structure at one end Labeling studies have shown such proteins to be located at one end and along lateral margins of the centriolar cylinder, forming a mass the shape of a tube. See Fig. 2 in article by Ou et al. lockwasher shape cap g-tubulin ring complex g-Tubulin, which is homologous to a & b tubulins, nucleates microtubule assembly within the centrosome. Several (12-14) copies of g-tubulin associate in a complex with other proteins called “grips” (gamma ring proteins). This g-tubulin ring complex is seen by EM to have an open ring-like structure resembling a lock washer, capped on one side. Microtubules nucleated by the g-tubulin ring complex appear capped at one end, assumed from other data to be the minus end. lockwasher shape cap g-tubulin ring complex Polymerization at the minus end of these microtubules is inhibited. Grip proteins of the cap may be involved in mediating binding to the centrosome. Phosphorylation of a conserved tyrosine residue of g-tubulin has been shown to regulate microtubule nucleation in yeast cells. Website with micrographs & diagrams. centrosome astral microtubule polar microtubule chromosomal microtubule During cell division, the duplicated centrosome helps to organize the mitotic spindle. MTOC nucleus microtubules During interphase, the centrosome (MTOC) is usually located near the nucleus. Microtubules grow out from the MTOC, forming a hub & spoke array, even during interphase. MTOC With minus ends of most microtubules anchored in the centrosome, microtubules grow & shrink mainly through addition & loss of tubulin heterodimers at their plus ends. nucleus microtubules A sub-population of microtubules with free minus ends exists in some cells. These may arise by breakage or cleavage of microtubules. Dynamic instability: slower Microtubules growth microtubule may grow length steadily & then shrink rapidly by rapid loss of tubulin disassembly dimers at the time plus end. The rapid disassembly is called catastrophe. In vitro, a tendency to grow or shrink depends on [tubulin]. As microtubules grow, tubulin dimers are depleted. Below a critical tubulin concentration, rapid shrinkage at the plus end has been attributed to loss of a GTP cap. Hydrolysis of GTP by b-tubulin, as polymerization brings it into contact with a-tubulin, takes time. b-GTP a-GTP A rapidly growing microtubule may accumulate a few layers of tubulin-GTP at the (+) end. b-GDP a-GTP A GTP cap stabilizes the plus end of a microtubule. + seam microtubule 3-start helix If the concentration of tubulin heterodimers is low, dissociation of tubulin-GTP may expose tubulin-GDP at the plus end, causing that end to be unstable. Rapid shrinkage ensues. Fraying or curving of protofilaments is observed at the ends of rapidly disassembling microtubules. This may be due to a change in conformation when b-subunits at the plus end have bound GDP instead of GTP. protofilament microtubule during rapid shortening at the plus end Tubulin heterodimers with GDP on the b subunit form ring shaped assemblies in vitro. Straight protofilaments form only when both tubulins have bound GTP. Dynamic instability of microtubules in vivo is regulated by interaction with other proteins. E.g., during prophase of mitosis, microtubules grow out from the centrosome. If the plus end of a microtubule makes contact with a chromosome, the end becomes stabilized. Otherwise rapid disassembly at the plus end ensues, and the tubulin dimers are available for growth of another microtubule. A website of the Borisy lab has movies depicting microtubule instability. See, e.g., movie #1 on centrosomal control of microtubule dynamics. MAPs (microtubule-associated proteins) are a diverse class of proteins that bind to microtubules. Binding of MAPs may be regulated by phosphorylation, which causes some MAPs to detach from microtubules. +TIPS, or plus-end tracking proteins, associate with the plus ends of microtubules. Many +TIPs are motor proteins. Some mediate interaction with the actin cytoskeleton in the cell cortex, adjacent to the plasma membrane. Some +TIPS regulate microtubule dynamics and stability at the plus end. +TIPS (plus-end binding proteins) that stabilize or promote growth of microtubules include, e.g.: Members of the XMAP215 family of proteins stabilize plus ends of microtubules, preventing catastrophic shrinkage and promoting microtubule growth. CLASPs are proteins that promote addition of tubulin dimers at the plus end and inhibit catastrophe. They are associated with kinetochores, the complexes that link plus ends of mitotic spindle microtubules to chromosomes. Catastrophe-promoting proteins (catastrophins) bind to plus ends of microtubules & promote dissociation of tubulin dimers. They may activate GTP hydrolysis or induce a curved protofilament conformation. E.g., MCAK, a member of the kinesin family of proteins, promotes dissociation of tubulin dimers at the kinetochore, as kinetochore-linked microtubules shorten in anaphase of mitosis. Shortening of chromosomal spindle microtubules in anaphase A ()() kinetochore free tubulin In vitro, MCAK can cause microtubules to shrink at both ends. Movie of microtubule shortening after MCAK addition (video supplement #1, article of Helenius et al). Other proteins that promote microtubule disassembly: Stathmin is a microtubule destabilizing protein that increases in abundance in some cancer cells. It binds to tubulin heterodimers, decreasing their availability for polymerization. Stathmin is inhibited by phosphorylation. Katanin severs microtubules, generating: • new plus ends that lack a stabilizing GTP cap • minus ends that are not stabilized by being capped by g-ring complexes of the centrosome. KLP10A & related members of the Kin I subfamily of kinesins associate with uncapped minus ends of microtubules at the spindle poles during mitosis. They promotes dissociation of tubulin dimers at the poles of the cell, contributing to: • treadmilling (flow of subunits toward the poles) • shortening of kinetochore-linked microtubules during anaphase of mitosis. Some MAPs cross-link adjacent microtubules or link microtubules to membranes or to intermediate filaments. The length of intervening segments between binding domains in particular MAPs may determine the spacing of microtubules in parallel arrays. Some examples: Type I MAPs, in axons & dendrites of nerve cells & in some non-neural cells, have several repeats of the sequence KKEX (Lys-Lys-Glu-X) that binds to negatively charged tubulin domains. Type II MAPs (e.g., MAP4 & Tau), in axons, dendrites & non-neural cells, have 3-4 repeats of an 18-residue sequence that binds tubulin. Toxins & Drugs Some toxins and drugs (all of which inhibit mitosis) affect polymerization or depolymerization of tubulin: Taxol, an anti-cancer drug, stabilizes microtubules. Colchicine binds tubulin & blocks polymerization. Microtubules depolymerize at high [colchicine]. Vinblastine causes depolymerization and formation of vinblastine-tubulin paracrystals. Nocodazole causes depolymerization of microtubules.