JAGGED Controls Growth Anisotropy and Coordination between Cell Size and Cell Cycle during Plant Organogenesis

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Highlights? JAGGED (JAG) is required for growth of initiating floral organs in Arabidopsis ? JAG decouples cell cycle from cell growth during organ emergence ? JAG promotes fast, anisotropic growth when floral organs emerge from the meristem ? JAG directly represses meristem identity genes     

Growth During the Bacterial Cell Cycle: Analysis of Cell Size Distribution

Cell volume distributions were determined electronically for steady-state cultures of Escherichia coli, Bacillus megaterium, Bacillus subtilis, and Salmonella typhimurium by use of a Coulter transducer-multichannel analyzer system of good resolution. All of the cell volume distributions had the same general shape, even though cultures were grown at widely different rates. Some results were independent of any particular growth model. Both the variability in the volumes of dividing cells and the fraction of constricted and unseparated doublet cells increased with growth rate. The greater separation to single cells at slow growth rates is in agreement with the general finding that filamentous and hyphal forms are greatly reduced in slowly growing chemostat cultures. The distributions were fitted equally well by simple models which assumed that cell growth was either linear or exponential throughout the entire cell cycle. It is concluded that methods of determining growth rate by analysis of distributions of bacterial volumes do not yet have sufficient resolution to distinguish between a variety of alternative models for growth of bacteria.     

植物细胞周期及其调控

概述了植物细胞周期的特点及其调控.     

细胞周期因子与植物根系发育

植物根系的发育是一个非常复杂且被精确调控的过程,受到多种信号的调控,其中对细胞分裂水平调控的研究已经成为细胞生物学研究的热点之一.文章介绍了植物细胞周期因子和植物根系发育相关的细胞周期调控机制以及根系细胞周期激素调节的研究进展.     

Plant Cell Growth in Tissue

Cell walls are part of the apoplasm pathway that transports water, solutes, and nutrients to cells within plant tissue. Pressures within the apoplasm (cell walls and xylem) are often different from atmospheric pressure during expansive growth of plant cells in tissue. The previously established Augmented Growth Equations are modified to evaluate the turgor pressure, water uptake, and expansive growth of plant cells in tissue when pressures within the apoplasm are lower and higher than atmospheric pressure. Analyses indicate that a step-down and step-up in pressure within the apoplasm will cause an exponential decrease and increase in turgor pressure, respectively, and the rates of water uptake and expansive growth each undergo a rapid decrease and increase, respectively, followed by an exponential return to their initial magnitude. Other analyses indicate that pressure within the apoplasm decreases exponentially to a lower value after a step-down in turgor pressure, which simulates its behavior after an increase in expansive growth rate. Also, analyses indicate that the turgor pressure decays exponentially to a constant value that is the sum of the critical turgor pressure and pressure within the apoplasm during stress relaxation experiments in which pressures within the apoplasm are not atmospheric pressure. Additional analyses indicate that when the turgor pressure is constant (clamped), a decrease in pressure within the apoplasm elicits an increase in elastic expansion followed by an increase in irreversible expansion rate. Some analytical results are supported by prior experimental research, and other analytical results can be verified with existing experimental methods.Cell walls perform many functions for plant, algal, and fungal cells. Physical and chemical protection from the environment and physical support for cells and organs are obvious functions. Cell walls also withstand the stresses imposed by turgor pressure and deform irreversibly and reversible (elastically) during expansive growth. Irreversible wall deformations during expansive growth control cell enlargement, size, and shape. Growing and mature (nongrowing) cell walls undergo elastic deformations after changes in turgor pressure caused by changes in water status and environmental conditions. Elastic wall deformations are fundamental to the water relations of plant, algal, and fungal cells. For plant cells in tissues and organs, cell walls are part of the apoplasm pathway that transports water, solutes, and nutrients to cells.Importantly, pressures within the apoplasm (cell walls and xylem) are frequently different from atmospheric pressure during expansive growth of plant cells in tissues and organs. Lower pressures (tensions) are related to transpiration rates from plant organs and to expansive growth of cells in plant organs, e.g. Boyer (1967, 2001), Molz and Boyer (1978), Nonami and Boyer (1987, 1993), Nonami and Hashimoto (1996), Passioura and Boyer (2003), Boyer and Silk (2004), Koch et al. (2004), Wiegers et al. (2009), and the references within. Higher pressures (root pressures) occur during the spring when the soil is well hydrated (e.g. Kramer, 1932). Bleeding sap from cuts and broken stems is evidence of root pressure. Also, higher pressures may occur diurnally, during the night when transpiration rates are low (e.g. Tang and Boyer, 2008). Guttation drops on leaves in the morning are evidence of these higher pressures.Prior research indicates that a significant amount of chemistry and molecular biology occur within cell walls undergoing irreversible deformation during expansive growth (e.g. Cosgrove, 2005; Boyer, 2009). Two questions arise. First, how do pressures within the wall that are different from atmospheric pressure affect the turgor pressure, water uptake, and growth rate of cells in plant organs such as roots, stems, and leaves? Second, how are relevant chemical reactions affected by lower and higher pressures within the wall? The analyses conducted in this article focus on the first question.Previously, equations derived by Lockhart (1965) for wall deformation and water uptake (Growth Equations) were augmented with terms for elastic wall deformation (Ortega, 1985) and transpiration (Ortega et al., 1988). In this article, the previously established Augmented Growth Equations (Ortega, 1985, 1990, 1994, 2004; Ortega et al., 1988; Geitmann and Ortega, 2009) are modified to evaluate the turgor pressure, water uptake, and expansive growth of plant cells in tissue when pressures within the apoplasm are lower and higher than atmospheric pressure. In addition, the pressure within the apoplasm is evaluated after turgor pressure in cells decrease, thus simulating the condition produced by an increase in expansive growth rate of cells in plant tissues and organs. Also, the modified equations are used to determine how the results of stress relaxation experiments conducted on growing plant organs are affected by pressures within the apoplasm that are not atmospheric pressure. Last, the expansive growth of a plant cell is evaluated when pressure within the apoplasm undergoes a semi-instantaneous change while the turgor pressure remains constant, i.e. clamped. Some analytical results are supported by prior experimental research, and some analytical results can be verified with existing experimental methods.     

Control of Cell Cycle and Cell Growth by Molecular Chaperones

Cells adapt their size to both intrinsic and extrinsic demands and, among them, those that stem from growth and proliferation rates are crucial for cell size homeostasis. Here we revisit mechanisms that regulate cell cycle and cell growth in budding yeast. Cyclin Cln3, the most upstream activator of Start, is retained at the endoplasmic reticulum in early G1 and released by specific chaperones in late G1 to initiate the cell cycle. On one hand, these chaperones are rate-limiting for release of Cln3 and cell cycle entry and, on the other hand, they are required for key biosynthetic processes. We propose a model whereby the competition for specialized chaperones between growth and cycle machineries could gauge biosynthetic rates and set a critical size threshold at Start.     

Rosiglitazone Suppresses Glioma Cell Growth and Cell Cycle by Blocking the Transforming Growth Factor-Beta Mediated Pathway

Glioma is one of the most malignant tumors in the central nervous system. As a peroxisome proliferator-activated receptor γ (PPAR-γ) activator, the thiazolidinediones (TZDs) induce growth arrest and cell death in a broad spectrum of tumor cells. In this study, we investigated the role of rosiglitazone in glioma cells. We found that rosiglitazone, a member of TZDs, suppresses growth of human glioma cell lines U87 and U251. Rosiglitazone also induces cell cycle arrest and apoptosis, which may be the mechanism of its anti-proliferation effect. Next, we found that rosiglitazone suppresses the expression of TGF-beta and its receptor TGF-betaR2, and suppresses phosphorylation of Smad3. Rosiglitazone also inhibits formation of the Smad3/Smad4 complex. Furthermore, Rosiglitazone affects the expression of Smad3/Smad4 associated regulators of gene expression, including p21 and c-Myc. These results suggest that rosiglitazone suppresses growth and cell cycle of human glioma cells by blocking the TGF-beta mediated pathway.     

A Microbial Avenue to Cell Cycle Control in the Plant Superkingdom

Research in yeast and animals has resulted in a well-supported consensus model for eukaryotic cell cycle control. The fit of this model to early diverging eukaryotes, such as the plant kingdom, remains unclear. Using the green alga Chlamydomonas reinhardtii, we developed an efficient pipeline, incorporating robotics, semiautomated image analysis, and deep sequencing, to molecularly identify >50 genes, mostly conserved in higher plants, specifically required for cell division but not cell growth. Mutated genes include the cyclin-dependent kinases CDKA (resembling yeast and animal Cdk1) and the plant-specific CDKB. The Chlamydomonas cell cycle consists of a long G1 during which cells can grow >10-fold, followed by multiple rapid cycles of DNA replication and segregation. CDKA and CDKB execute nonoverlapping functions: CDKA promotes transition between G1 and entry into the division cycle, while CDKB is essential specifically for spindle formation and nuclear division, but not for DNA replication, once CDKA-dependent initiation has occurred. The anaphase-promoting complex is required for similar steps in the Chlamydomonas cell cycle as in Opisthokonts; however, the spindle assembly checkpoint, which targets the APC in Opisthokonts, appears severely attenuated in Chlamydomonas, based on analysis of mutants affecting microtubule function. This approach allows unbiased integration of the consensus cell cycle control model with innovations specific to the plant lineage.     

KSHV Manipulates Notch Signaling by DLL4 and JAG1 to Alter Cell Cycle Genes in Lymphatic Endothelia

Increased expression of Notch signaling pathway components is observed in Kaposi sarcoma (KS) but the mechanism underlying the manipulation of the canonical Notch pathway by the causative agent of KS, Kaposi sarcoma herpesvirus (KSHV), has not been fully elucidated. Here, we describe the mechanism through which KSHV directly modulates the expression of the Notch ligands JAG1 and DLL4 in lymphatic endothelial cells. Expression of KSHV-encoded vFLIP induces JAG1 through an NFκB-dependent mechanism, while vGPCR upregulates DLL4 through a mechanism dependent on ERK. Both vFLIP and vGPCR instigate functional Notch signalling through NOTCH4. Gene expression profiling showed that JAG1- or DLL4-stimulated signaling results in the suppression of genes associated with the cell cycle in adjacent lymphatic endothelial cells, indicating a role for Notch signaling in inducing cellular quiescence in these cells. Upregulation of JAG1 and DLL4 by KSHV could therefore alter the expression of cell cycle components in neighbouring uninfected cells during latent and lytic phases of viral infection, influencing cellular quiescence and plasticity. In addition, differences in signaling potency between these ligands suggest a possible complementary role for JAG1 and DLL4 in the context of KS.     

One is Nothing without the Other: Theoretical and Empirical Analysis of Cell Growth and Cell Cycle Progression

Small, fast-growing bacteria make ideal subjects for genetic and quantitative analysis alike. Long the darling of theoreticians, efforts to understand the relationship between cell growth and cell cycle progression in bacterial systems have been propelled by modelers and empiricist in equal measure. Taking a historical approach, here we break down early work in this area, the impact it had on how the bacterial cell cycle is understood and interrogated, and changes brought by the advent of high-throughput techniques for the analysis of individual bacterial cells in culture.     

Changes in Triterpenoid Content during the Growth Cycle of Cultured Plant Cells

Similar changes in the pentacyclic triterpenoid contents wereobserved during the growth cycle of Datura innoxia, Luffa cylindricaand Lycopersicon esculentum seedling callus cells in batch culture.Triterpenoid contents decreased for several days after callusinoculation, then increased rapidly during the mid and lateexponential phases of growth. (Received May 28, 1984; Accepted September 13, 1984)     

Interaction of the Circadian Cycle with the Cell Cycle in Pyrocystis fusiformis

Dividing pairs or single cells of the large dinoflagellate, Pyrocystis fusiformis Murray, were isolated in capillary tubes and their morphology was observed over a number of days, either in a light-dark cycle or in constant darkness. Morphological stages were correlated with the first growth stage, G₁, DNA synthesis, S, the second growth stage, G₂, mitosis, M, and cytokinesis, C, segments of the cell division cycle. The S phase was identified by measuring the nuclear DNA content of cells of different morphologies by the fluorescence of 4′, 6-diamidino-2-phenylindole dichloride.

Cells changed from one morphological stage to the next only during the night phase of the circadian cycle, both under light-dark conditions and in continuous darkness. Cells in all segments of the cell division cycle displayed a circadian rhythm in bioluminescence. These findings are incompatible with a mechanism for circadian oscillations that invokes cycling in G_q, an hypothesized side loop from G₁. All morphological stages, not only division, appear to be phased by the circadian clock.