Regulation of cell division and cell enlargement by turgor pressure

Isolated radish (Raphanus sativus L., var. Red Prince) cotyledons were incubated in growth medium plus graded concentrations of mannitol (−1 to −16 bars) for 28 hours. At the end of the incubation period, turgor pressures were measured using thermocouple psychrometers. Cell division, as measured by DNA increase, was greatly stimulated by increasing turgor from 5 to 6 bars. Cell enlargement was stimulated as turgor increased above 3 bars. The critical turgor pressure for increased cell division thus appeared significantly greater than that for increased cell enlargement.     

Regulation of prostate cancer cell invasion by modulation of extra- and intracellular redox balance

Recent metabolic profiles of human prostate cancer tissues showed a significant increase in cysteine (Cys) and a significant decrease in reduced glutathione (GSH) during cancer progression from low- to high-grade Gleason scores. Cys is primarily localized extracellularly, whereas GSH is present mostly inside the cell. We hypothesized that extra- or intracellular redox state alterations differentially regulate cell invasion in PC3 prostate carcinoma cells versus PrEC normal prostate epithelial cells. Cells were exposed to media with calculated Cys/CySS redox potentials (E(h)CySS) ranging from -60 to -180mV. After 3h exposure to a reducing extracellular redox state (E(h)CySS=-180mV), matrix metalloprotease (MMP), gelatinase, and NADPH oxidase activities increased, correlating with increases in cell invasion, cell migration, and extracellular hydrogen peroxide levels in PC3 cells but not PrECs. Knockdown of NADPH oxidase or MMP with silencing RNAs during cultivation with E(h)CySS=-180mV medium significantly decreased PC3 cell invasion. Modulation of extra- and intracellular redox states by exposure of PC3 cells to Cys/CySS-free medium (approx E(h)CySS=-87mV) containing 500μMN-acetylcysteine resulted in a more reducing intracellular redox state and a significant decrease in cell invasive ability. The decrease in PC3 cell invasion induced by these conditions correlated with a decrease in MMP activity. Our studies demonstrated that an extracellular redox state that was more reducing than a physiologic microenvironment redox state increased PC3 cancer cell invasive ability, whereas an intracellular redox environmental that was more reducing than an intracellular physiologic redox state inhibited PC3 cell invasive ability.     

Regulation of cell division and malignant transformation

The problem of regulation of cell division is essentially a problem of understanding regulation of transition from the resting state of a cell to the dividing state and vice versa. In malignancy the ability to revert back to a normal resting state is impaired. A model is presented which attempts to explain the control of the above transitions through control of uptake of essential nutrients by a transport-inhibitory protein. Experimental evidence in favour of the model is given.     

Regulation of cell division in E. coli

Recent investigation of some old cell division mutants of E. coli suggests that genes playing central roles in the regulation of division have been identified. The results suggest that cell division is triggered when a critical level of a single protein, FtsZ, is attained. The activity of this protein is channelled to the new division site by the activity of the min locus, which blocks access to old sites. Continued study of these genes should yield further insights into the cell division process.     

Mitosis: Regulation and organization of cell division

Modern views on genetic, cytological and molecular bases of the structure and regulation of preparing and implementing mitotic chromosome segregation are discussed.Translated from Genetika, Vol. 40, No. 12, 2004, pp. 1589–1608.Original Russian Text Copyright © 2004 by Lebedeva, Fedorova, Trunova, Omelyanchuk.     

Regulation of store-operated calcium entry during cell division

Store-operate Ca2+ channels gate Ca2+ entry into the cytoplasm in response to the depletion of Ca2+ from endoplasmic reticulum Ca2+ stores. The major molecular components of store-operated Ca2+ entry are STIM (stromal-interacting molecule) 1 (and in some instances STIM2) that serves as the endoplasmic reticulum Ca2+ sensor, and Orai (Orai1, Orai2 and Orai3) which function as pore-forming subunits of the store-operated channel. It has been known for some time that store-operated Ca2+ entry is shut down during cell division. Recent work has revealed complex mechanisms regulating the functions and locations of both STIM1 and Orai1 in dividing cells.     

Regulation of asymmetric cell division in the epidermis

For proper tissue morphogenesis, cell divisions and cell fate decisions must be tightly and coordinately regulated. One elegant way to accomplish this is to couple them with asymmetric cell divisions. Progenitor cells in the developing epidermis undergo both symmetric and asymmetric cell divisions to balance surface area growth with the generation of differentiated cell layers. Here we review the molecular machinery implicated in controlling asymmetric cell division. In addition, we discuss the ability of epidermal progenitors to choose between symmetric and asymmetric divisions and the key regulatory points that control this decision.     

Regulation of mouse spermatogonial stem cell self-renewing division by the pituitary gland

Spermatogenesis originates in spermatogonial stem cells, which have the unique mode of replication. It is considered that a single stem cell can produce two stem cells (self-renewing division), one stem and one differentiating (asymmetric division), or two differentiating cells (differentiating division). However, little is known regarding how each type of division is regulated. In this investigation, we focused on the analysis of self- renewing division and examined the effect of the pituitary gland using two models of stem cell self-renewing division. In the first experiment using newborn mice, the administration of GnRH- analogue, which represses the release of gonadotropin, reduced the number of stem cells during postnatal testicular development, suggesting that the pituitary gland enhances stem cell self- renewing division. In the second experiment, however, the number of stem cells increased dramatically in hypophysectomized adult recipients after spermatogonial transplantation. Thus, the pituitary gland affects the self-renewing division of stem cells, but these contradictory results suggest that its role may be different depending on the stage of the testicular development.     

Regulation of embryonic cell division by a Xenopus gastrula-specific protein kinase.

We describe a novel protein kinase, Pk9.7, and its role in cell division in the Xenopus embryo. Pk9.7 is transcribed only during blastula and gastrula stages. Expression of Pk9.7 in Xenopus oocytes induces meiotic maturation, while overexpression in embryos blocks blastomere cleavage in a MAP kinase-independent fashion. In both Pk9.7-injected oocytes and mitotic cells of cleavage-blocked embryos, chromosomes appear detached from abnormal spindles, and in oocytes additional microtubule structures are formed, suggesting that one function of Pk9.7 is to regulate formation of, and chromosome attachment to, the spindle. Consistent with this, Pk9.7 co-immunoprecipitates tubulin and phosphorylates it in vitro. Pk9.7 expression coincides with the switch from maternal to zygotic control of the cell cycle, and with the switch from microtubule independence to microtubule dependence. Our results suggest that Pk9.7 plays a role in these processes.     

Regulation of cell division: stop the SIN!

A novel mechanism, centered on the Polo-like kinase Plo1p and Dma1p - a protein with a RING finger and an FHA-domain - prevents cytokinesis as long as the spindle checkpoint is active.     

Regulation of VEGF, MMP-9 and metastasis by CXCR4 in a prostate cancer cell line

To investigate the mechanisms involved in PCa (prostate cancer) metastasis and CXCR4 (CXC chemokine receptor-4)-mediated VEGF (vascular endothelial growth factor) and MMP-9 (matrix metalloproteinase-9) expression, we used lentivirus-mediated RNAi (RNA interference) to reduce the expression of CXCR4 in a PCa cell line. We found that the silencing of CXCR4 led to a significant down-regulation of VEGF and MMP-9 at both the mRNA and protein levels compared with the control in vitro. Using an animal model, we confirmed that CXCR4 silencing via subcutaneous injection could reduce tumour growth as well as inhibit metastasis, particularly bone metastasis, of PCa. Using in vivo immunohistochemistry, we also found that the expression of VEGF and MMP-9 were reduced by the knockdown of CXCR4 in the primary tumours of mice. Collectively, our results indicate that CXCR4 plays an important role in PCa metastasis through the up-regulation of VEGF and MMP-9. These findings may aid future intervention strategies.     

Regulation of the plane of cell division in vacuolated cells

Summary In small leaf explants fromNautilocalyx lynchii (Hook. f.) Sprague (Gesneriaceae) the vacuolated epidermal cells divide after 3–4 days. Most cells divide periclinally, but longitudinal and transverse divisions are also found. Before mitosis the cells form a phragmosome (PS), a cytoplasmic structure which contacts the cell cortex at the future division site. An experimental approach was used to find out at which time the plane of cell division becomes fixed: prior to or during the formation of a PS.When 3 day-old explants were divided into two parts by a longitudinal cut, a high percentage of the cells near the wound divided longitudinally. Cells which already had a PS at the time of wounding most often divided in the plane of the PS. Some of the cells with a non-longitudinal PS, however, formed a longitudinal cell wall after the replacement of the original PS by a longitudinal PS.The observations show that most cells which had not yet formed a PS could be induced to form a cell wall in a new direction. As soon as the formation of the PS had started, however, it became more difficult to induce a change in the plane of cell division. These results suggest that the division site is chosen during the formation of the PS.Abbreviations BMT band of microtubules - DIC differential interference contrast microscopy - l longitudinal - l-o longitudinal-oblique - MT microtubule - p periclinal - PM prometaphase - PPB preprophase band - PS phragmosome - t transverse - t-o transverse-oblique     

Regulation of cell division of mature B cells by ionomycin and phorbol ester.

The growth of a human B lymphoma cell line B104, an experimental model for mature B cells, was inhibited by ionomycin but not 12-O-tetradecanoylphorbol-13-acetate (TPA). Ionomycin inhibited B104 cells from entering into the M phase of the cell cycle without affecting DNA synthesis. The inhibition of cell division of B104 cells by ionomycin occurred within 24 h after stimulation. Because such a mode of action resembles that of anti-IgM antibodies, signals transduced by Ca2+ may be responsible for the inhibition of cell division of B104 cells by anti-IgM antibodies. Indeed, EGTA suppressed the inhibition of cell division of B104 cells caused not only by ionomycin, but also by anti-IgM antibody. Although TPA itself did not have any ability to promote the growth of B104 cells, it could cancel the inhibition of cell division of B104 cells by ionomycin and increase the proportion of B104 cells entering into the M phase of the cell cycle. Staphylococcus aureus Cowan I causes the greatest proliferation of normal human peripheral blood B cells during the period from 48 to 72 h after stimulation. When ionomycin was added to S. aureus Cowan I-stimulated peripheral blood B cells at 48 h of culture, it inhibited cell division during this period without affecting DNA synthesis. In the presence of TPA, this activity of ionomycin was suppressed, and the proportion of M-phase cells increased. These results suggest that cell division of mature B cells is regulated by the signals mediated by Ca2+ and protein kinase C in a mode quite different from that of regulation of DNA synthesis.