Bud Growth And Polarity

A basic problem in development is to understand the principles by which multicellular organisms determine the time and correct positions of new cells generating shape (patterning). This is the principle of polarity, seen at the level of an organism in the organization of head-and-foot structure of humans and animals, in the shoot-and-root system of plants, and so on. At the cellular level, polarity is observed in the plane of cell division as in the case of the Fucus zygote, where division plane of the nucleus in the rhizoid cell lies perpendicular to that in the thallus cell; in the organization of the nerve cells with dendrites at one end and axon at the other end; and in the structure of transporting epithelial cells lining our stomach and intestine with an apical and a basolateral end that separates two distinct compartments. The concept of polarity is equally prevalent in fundamental biological processes such as embryogenesis, where asymmetrical cleavage of the fertilized egg creates cells that follow distinct fates, or during communication between immune cells such as B and T-lymphocytes or during neurogenesis, where nerve cells are actively guided so that they reach and synapse at specific regions in the brain. Studies in the last four decades have revealed that the underlying mechanism behind all manifestations of polarity in unicellular or multicellular organisms lies in the generation of cellular asymmetry and a conserved mechanism involving cytoskeletal reorganization guides this process (Nelson, 2003).

Figure 6.4 A biochemical model of cell cycle regulation in eukaryotes. Each phase of the cycle is regulated by the timely expression of a distinct cyclin protein. Entry of cells into mitosis is controlled by successive phosphorylation by kinases and dephosphoryla-tion by phosphatases. The yeast cyclin-dependent kinase CDC28p is activated by phosphorylation of threonine-18 (T-18) and inhibited by phosphorylation of tyrosine-19 (Y 19). CLN2p commits the cell into START by activating CDC28. Once activated, CDC28p phosphorylates CLN2p resulting in dissociation of the complex. CDC28 is inactivated by dephosphorylation and phosphorylated CLN2p is degraded. CLB5 and CLB2 proteins initiate S-phase and M-phase respectively. The end of M-phase is marked by rapid degradation of CLB2 and dephosphorylation of CDC28 kinase.

Figure 6.4 A biochemical model of cell cycle regulation in eukaryotes. Each phase of the cycle is regulated by the timely expression of a distinct cyclin protein. Entry of cells into mitosis is controlled by successive phosphorylation by kinases and dephosphoryla-tion by phosphatases. The yeast cyclin-dependent kinase CDC28p is activated by phosphorylation of threonine-18 (T-18) and inhibited by phosphorylation of tyrosine-19 (Y 19). CLN2p commits the cell into START by activating CDC28. Once activated, CDC28p phosphorylates CLN2p resulting in dissociation of the complex. CDC28 is inactivated by dephosphorylation and phosphorylated CLN2p is degraded. CLB5 and CLB2 proteins initiate S-phase and M-phase respectively. The end of M-phase is marked by rapid degradation of CLB2 and dephosphorylation of CDC28 kinase.

The budding and the fission yeast are attractive systems to understand cellular asymmetry at the molecular level. First, S. cerevisiae shows polarized growth at every cell division by taking a decision where to produce the bud. Second, the complex process is genetically tractable. The budding pattern is easily observed by staining yeast cells with a fluorescent dye calcofluor, which fluoresces after binding to cell wall chitin. Bud scars are especially rich in chitin and fluoresce brightly (Figure 6.5).

At every division cycle, S. cerevisiae selects the site of a new bud in a spatially distinct pattern (Freifelder, 1960). Haploid a or a cells choose bud sites in an axial pattern in which mother and daughter cells bud adjacent to their prior mother-bud junction. On the other hand, diploid a or a cells choose sites in a bipolar pattern in which mother cell buds either adjacent to the last daughter or at the pole opposite the last daughter. The daughter, however, always buds at the pole opposite its mother. The two distinct patterns of budding are shown in Figure 6.5.

In the original screen (Chant and Herskowitz, 1991), haploid yeast cells were mutagenized and plated on soft agar plates. Mutants defective in axial budding pattern were

Birth scar

Birth scar

Axial pattern

Diploid a/a

Axial pattern

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