TL;DR: This review focuses on the wall because it is the major control point for cell enlarge- ment and some of the key processes that may be involved in wall enlargement are summarized in Figure 4.
Abstract: SUMMARY AND PERSPECTIVE The enlargement of plant cells involves the coordinate con- trol of wall synthesis and expansion, solute and water trans- port, membrane synthesis, Golgi secretion, ion transport, and many other processes. In this review, I have focused on the wall because it is the major control point for cell enlarge- ment. Some of the key processes that may be involved in wall enlargement are summarized in Figure 4. I offer the following speculative picture as a tentative working model for the control of wall expansion. The primary wall is initially secreted and assembled in a form that is me- chanically tough yet has “hot spots” where expansin can weaken microfibril-matrix adhesion. Expansin activity, which is modulated both by secretion of the protein to the wall and by changes in the pH and redox potential of the wall, in- duces the stress relaxation and polymer creep needed for wall enlargement and water uptake by the cell. By altering Synthesis & secretion secretion of wall polysaccharides and proteins
TL;DR: It is proposed that the range of DNA:cytoplasm ratio that supports optimal cell function is limited and that ratios outside these bounds contribute to aging.
TL;DR: It is concluded that proliferating mammalian cells have an intrinsic mechanism that maintains cell size, and growth rate is size-dependent throughout the cell cycle.
Abstract: A long-standing question in biology is whether there is an intrinsic mechanism for coordinating growth and the cell cycle in metazoan cells. We examined cell size distributions in populations of lymphoblasts and applied a mathematical analysis to calculate how growth rates vary with both cell size and the cell cycle. Our results show that growth rate is size-dependent throughout the cell cycle. After initial growth suppression, there is a rapid increase in growth rate during the G1 phase, followed by a period of constant exponential growth. The probability of cell division varies independently with cell size and cell age. We conclude that proliferating mammalian cells have an intrinsic mechanism that maintains cell size.
TL;DR: In this paper, the authors describe a mechanism by which C. neoformans evades host phagocytosis to allow survival of a subset of the population at early stages of infection.
Abstract: Cryptococcus neoformans is a common life-threatening human fungal pathogen. The size of cryptococcal cells is typically 5 to 10 µm. Cell enlargement was observed in vivo, producing cells up to 100 µm. These morphological changes in cell size affected pathogenicity via reducing phagocytosis by host mononuclear cells, increasing resistance to oxidative and nitrosative stress, and correlated with reduced penetration of the central nervous system. Cell enlargement was stimulated by coinfection with strains of opposite mating type, and ste3aΔ pheromone receptor mutant strains had reduced cell enlargement. Finally, analysis of DNA content in this novel cell type revealed that these enlarged cells were polyploid, uninucleate, and produced daughter cells in vivo. These results describe a novel mechanism by which C. neoformans evades host phagocytosis to allow survival of a subset of the population at early stages of infection. Thus, morphological changes play unique and specialized roles during infection.
TL;DR: In this paper, a plant homologue of APC activators involved in mitotic cyclin degradation, called ccs52, was identified from Medicago sativa root nodules, which exhibit the highest degree of endopolyploidy in this plant.
Abstract: Plant organs develop mostly post-embryonically from persistent or newly formed meristems. After cell division arrest, differentiation frequently involves endoreduplication and cell enlargement. Factors controlling transition from mitotic cycles to differentiation programmes have not been identified yet in plants. Here we describe ccs52, a plant homologue of APC activators involved in mitotic cyclin degradation. The ccs52 cDNA clones were isolated from Medicago sativa root nodules, which exhibit the highest degree of endopolyploidy in this plant. ccs52 represents a small multigenic family and appears to be conserved in plants. Overexpression of ccs52 in yeast triggered mitotic cyclin degradation, cell division arrest, endoreduplication and cell enlargement. In Medicago, enhanced expression of ccs52 was found in differentiating cells undergoing endoreduplication. In transgenic M.truncatula plants, overexpression of the ccs52 gene in the antisense orientation resulted in partial suppression of ccs52 expression and decreased the number of endocycles and the volume of the largest cells. Thus, the ccs52 product may switch proliferating cells to differentiation programmes which, in the case of endocycles, result in cell size increments.