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Figure 7

Figure 7. From: Morphogenesis and the Cell Cycle.

Swe1p degradation pathway. Swe1p shuttles in and out of the nucleus and can be recruited to the mother-bud neck by a hierarchy of interactions involving septins, Hsl1p, and Hsl7p. Hsl1p is activated by Elm1p, another neck-localized kinase. At the neck, Swe1p is phosphorylated at multiple sites by Cdc5p, which is thought to target Swe1p for degradation. Phosphorylation of Swe1p by Clb-Cdc28p (which may occur in the nucleus, in the cytoplasm, or at the neck) primes Swe1p for subsequent phosphorylation by Cdc5p.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 1

Figure 1. From: Morphogenesis and the Cell Cycle.

Morphogenetic events of the cell cycle. The four major morphogenetic events are (1) polarization in late G1, triggered by Cln1,2p-Cdc28p; (2) the apical-isotropic switch in early G2, triggered by Clb1,2p-Cdc28p; (3) breakdown of mother-bud asymmetry in late mitosis (trigger unknown); and (4) refocusing of growth toward the neck following mitotic exit, triggered by Clb-Cdc28p inactivation. Actin (red), septin (green), and Cdc42p (blue) localization during the cell cycle is indicated.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 6

Figure 6. From: Morphogenesis and the Cell Cycle.

The morphogenesis checkpoint. (A) During an unperturbed cell cycle, bud formation is coincident with DNA replication, and by the time of nuclear division, a bud is ready to receive the daughter nucleus. (B) Stresses can temporarily halt bud formation, and if the cell cycle continued unabated, cells would become binucleate. (C) In reality, delays in bud formation trigger compensatory G2 delays in the cell cycle through the morphogenesis checkpoint. Reprinted from Lew, D.J., 2003 The morphogenesis checkpoint: How yeast cells watch their figures, Curr. Opin. Cell Biol., 15:6 648–653, with permission from Elsevier.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 8

Figure 8. From: Morphogenesis and the Cell Cycle.

Hsl1p: a checkpoint sensory kinase. (A) Domain organization of Hsl1p. (B) Septins form a ring in unbudded cells adjacent to a locally flat plasma membrane (left), which is converted to a collar adjacent to a locally more tubular plasma membrane upon bud emergence (right). (C) When shmoo-shaped yeast are released into the cell cycle but prevented from budding (due to actin depolymerization), septins form rings (green) in either locally flat (left) or locally tubular (right) plasma membrane geometries. Both rings recruit Hsl1p, but only those inside the shmoo recruit Hsl7p (purple), suggesting that Hsl1p can respond to local membrane geometry.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 3

Figure 3. From: Morphogenesis and the Cell Cycle.

Cdc42p localization. A localized GEF (red line along the cortex) can lead to local GTP loading of Cdc42p (blue circles). (A) Without further assistance, GDP-Cdc42p (open circles) diffusion into the patch is balanced by GTP-Cdc42p diffusion away from the patch, so the overall Cdc42p concentration is constant. (B) By reversibly extracting GDP-Cdc42p (and not GTP-Cdc42p) from the membrane, GDI selectively increases the mobility of GDP-Cdc42p, facilitating rapid GDP-Cdc42p diffusion through the cytoplasm into the GEF-containing patch. GTP-Cdc42p diffusion remains slow, so there is a net accumulation of Cdc42p at the cortex with high GEF activity (red). (C) Cdc42p could also become concentrated at the GEF-containing patch by vesicle traffic on actin cables. This model assumes that Cdc42p somehow becomes highly concentrated into the vesicles.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 2

Figure 2. From: Morphogenesis and the Cell Cycle.

Polarity establishment. Bud-site selection (purple): prelocalized landmark proteins promote local GTP loading of Rsr1p, which recruits Cdc24p. In establishing polarity (blue), Cdc24p locally activates Cdc42p, employing positive feedback to generate and dynamically maintain a patch of highly concentrated GTP-Cdc42p at the cell cortex. During downstream events, localized GTP-Cdc42p employs various effectors to promote septin ring assembly (green), actin cable polarization (red), local exocytosis (yellow), and possibly also glucan synthesis and actin patch clustering. The downstream events also influence each other (only some of these links are shown) and together promote bud formation.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 4

Figure 4. From: Morphogenesis and the Cell Cycle.

Model for symmetry breaking. Bem1p (green) mediates formation of a complex containing a PAK (red) and the Cdc42p-directed GEF (yellow). This complex enables GTP-Cdc42p at the plasma membrane (blue) to initiate positive feedback by binding the PAK, so that the associated GEF exchanges GDP for GTP on neighboring Cdc42p (GDP-Cdc42p: open circles). Thus, a stochastic GTP loading of Cdc42p can lead to amplification of a cluster of GTP-Cdc42p. Panels depict a patch of cortex as seen from inside the cell. Reprinted from Kozubowski, L., K. Saito, J. M. Johnson, A. S. Howell, T. R. Zyla et al., 2008 Symmetry-Breaking Polarization Driven by a Cdc42p GEF-PAK Complex, Curr. Biol. 18:22 1719–1726, with permission from Elsevier.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.
Figure 5

Figure 5. From: Morphogenesis and the Cell Cycle.

Cytokinesis and cell separation. Sequential panels showing (from left to right): (Left) In late anaphase, actin cables and patches are dispersed and an actomyosin ring (red) forms in the center of the neck, recruited to and maintained at that site by the septin collar (green). (Second from left) Upon CDK inactivation, the septin collar splits to form two rings, and the actomyosin ring constricts, guiding a chitin synthase and its regulators (yellow) to deposit a primary septum (black). At around this time the actin cables and patches reorient toward the neck. (Third from left) Upon completion of the primary septum, mother and bud deposit a secondary septum (gray) on either side. (Right) Daughter cells synthesize and secrete chitinase (purple arrows), which degrades the primary septum (black) and several glucanases, which presumably degrade the edge cell wall connecting mother and bud (gray), allowing cell separation. (Bottom) A cross section through the central plane. The mother cell also contains a ring of chitinous cell wall (black) surrounding the neck, which is synthesized in late G1/S phase as a bud first emerges by a distinct chitin synthase. This ring remains as a bud scar following cell separation.

Audrey S. Howell, et al. Genetics. 2012 January;190(1):51-77.

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