Diploid yeast cells repeatedly polarize and bud from their poles, probably because of highly stable marks of unknown composition. Here, Rax2, a membrane protein, was shown to behave as such a mark. The Rax2 protein itself was inherited immutably at the cell cortex for multiple generations, and Rax2 was shown to have a half-life exceeding several generations. The persistent inheritance of cortical protein markers would provide a means to couple a cell's history to the future development of a precise morphogenetic form.

No abstract

Genomic studies in yeast have revealed that one eighth of genes are cell cycle regulated in their expression. Almost without exception, the significance of cell cycle periodic gene expression has not been tested. Given that many such genes are critical to cellular morphogenesis, we wanted to examine the importance of periodic gene expression to this process. The expression profiles of two genes required for the axial pattern of cell division, BUD3 and BUD10/AXL2/SRO4, are strongly cell cycle regulated. BUD3 is expressed close to the onset of mitosis. BUD10 is expressed in late G1. Through promotor-swap experiments, the expression profile of each gene was altered and the consequences examined. We found that an S/G2 pulse of BUD3 expression controls the timing of Bud3p localization, but that this timing is not critical to Bud3p function. In contrast, a G1 pulse of BUD10 expression plays a direct role in Bud10p localization and function. Bud10p, a membrane protein, relies on the polarized secretory machinery specific to G1 to be delivered to its proper location. Such a secretion-based targeting mechanism for membrane proteins provides cells with flexibility in remodeling their architecture or evolving new forms.

Bud-site selection in yeast offers an attractive system for studying cell polarity and asymmetric division. Haploids divide in an axial pattern, whereas diploids divide in a bipolar pattern. AXL1 is expressed in haploids but not diploids, and ectopic expression of AXL1 in diploids converts their bipolar budding pattern to an axial pattern. How Axl1 acts as a switch between the bipolar and axial patterns is not understood. Here we report that Axl1 localizes to the mother-bud neck and division site remnants of haploids. Axl1 is absent from diploids. Axl1 colocalizes with Bud3, Bud4, and Bud10, components of the axial landmark structure. This localization suggests that Axl1 couples the axial landmark with downstream polarity establishment factors. Consistent with such a role, Axl1 associated biochemically with Bud4 and Bud5. Genetic evidence suggests that Axl1 works with Bud3 and Bud4 to promote the activity of the Bud10 membrane protein. Given Axl1's suggested role in morphogenesis and cell fusion during mating, we also examined its localization during this process. Axl1 redistributes independently of the axial landmark to a tight cell surface dot at the tip of each mating projection. These dots are rapidly lost as prezygotes form.

Patterns of dendritic development in the neocortex of normal and reeler E15-17 mouse embryos are studied in Golgi impregnations. Interactions between dendrites and axon-rich strata appear to be critical determinants of dendritic morphology in both genotypes. Firstly, axon-dendrite proximity appears to stimulate dendritic sprouting, elongation and branching. Secondly, the position of the axon-rich strata with respect to the differentiating cell appears to determine the direction of dendritic growth and thereby the ultimate configuration of the dendritic arbor. With regard to specific cell configurations, a multipolar form is generated when the cell is embedded in an axon-rich zone. A monopolar or bipolar configuration is achieved when the cell lies in the axon-poor cortical plate and addresses and axon-rich stratum with one or both radially extended migratory processes. Such variations in the configuration of neurons with polar dendritic systems may be observed uniquely in the mutant cortex because axon-rich zones are stratified anomalously at multiple levels in the cortical plate. As a consequence, polar dendritic systems develop from either the superior, the inferior or both somatic poles of postmigratory cells. Pyramidal cells may, therefore, develop a normal upright or an abnormal "upside-down" disposition. Regardless of the orientation of the polar dendritic system, the axon emerges from the inferior aspect of the cell suggesting that there has been no rotation of the original migratory axis of the cell.