A Gradient of Positional Information in an Insect, Rhodnius

1972 ◽  
Vol 11 (3) ◽  
pp. 815-853 ◽  
Author(s):  
P. A. LAWRENCE ◽  
F. H. C. CRICK ◽  
M. MUNRO

Locke discovered a segmental gradient in Rhodnius which controls the polarity of the epidermal cell and gives positional information. The polarity is expressed by the orientation of folds in the adult epicuticle, which are aligned parallel to the contours in the gradient. It was later suggested that this gradient could be of a concentration of a diffusible substance. Because concentration gradients could be maintained in various ways we have simulated several models in the computer, and examined the results of rotating square pieces of model landscape through 90° and allowing diffusion. The gradient landscapes after different times and at equilibrium are plotted as contour maps and are compared with cuticle patterns from adult insects after rotation of square pieces of epidermis in larvae. One simple model, where the gradient depends only on the activities of a line of source cells at one end of the segment and a line of sink cells at the other, is eliminated by 2 observations: (1) the theoretical and experimental patterns are consistently different; and (2) when adults developing from operated larvae are made to form a supernumerary cuticle the first and second cuticles have almost identical patterns. This suggests that the gradient landscape has reached a steady state. In another model the cells are considered to act as homeostatic units in the gradient, and when moved to a new position they each attempt to maintain their original or ‘set’ concentration. Simulation of this model gives equilibrium patterns which are similar to the experimental results. It is suggested that the cells become ‘set’ at some stage in the cell cycle to the ambient concentration. This hypothesis predicts that after reaching initial equilibrium the pattern should change only if there are cell divisions. Adult insects are made to moult again under different conditions and it is found that pattern change is correlated with cell divisions. Locke also observed an asymmetry in the patterns after rotation of squares through 180°. Simulation showed that such asymmetry would result from each cell acting as a better homeostatic unit when moved one way in the gradient (for example when acting as a sink) than when moved the other (acting as a source). We do not claim that these comparisons eliminate all other classes of model, and present our conclusions in as general a form as possible.

Development ◽  
1989 ◽  
Vol 105 (1) ◽  
pp. 119-130 ◽  
Author(s):  
D.R. Primmett ◽  
W.E. Norris ◽  
G.J. Carlson ◽  
R.J. Keynes ◽  
C.D. Stern

This study provides evidence that cells destined to segment together into somites have a degree of cell division synchrony. We have measured the duration of the cell division cycle in somite and segmental plate cells of the chick embryo as 9.5 h using [3H]thymidine pulse- and-chase. Treatment of embryos with any of a variety of inhibitors known to affect the cell division cycle causes discrete periodic segmental anomalies: these anomalies appear about 6–7 somites after treatment and, in some cases, a second anomaly is observed 6 to 7 somites after the first. Since somites take 1.5 h to form, the 6- to 7- somite interval corresponds to about 9–10 h, which is the duration of the cell cycle as determined in these experiments. The anomalies are similar to those seen after heat shock of 2-day chick embryos. Heat shock and some of the other treatments induce the expression of heat-shock proteins (hsp); however, since neither the expression nor the distribution of these proteins relate to the presence or distribution of anomalies seen, we conclude that hsps are not responsible for the pattern of segmental anomalies observed. The production of periodic segmental anomalies appears to be linked to the cell cycle. A simple model is proposed, in which we suggest that the cell division cycle is involved directly in gating cells that will segment together.


A review is given of a theoretical investigation of the flow properties of fluids in which .the assumptions underlying the classical hydrodynamics of viscous fluids no longer holds. For an incompressible visco-inelastic fluid—or visco-elastic fluid in steady-state laminar flow— the stress-strain-velocity relations involve two physical parameters which may or may not depend on the state of flow. One of these is the viscosity and the other the normal stress coefficient. On a simple model of a concentrated high-polymer solution, it is shown that the normal stress coefficient may have an appreciable value. Finally, the manner in which the basic assumptions of the theory may be inapplicable to real concentrated high-poyimer solutions is discussed.


2007 ◽  
Vol 35 (2) ◽  
pp. 94-117 ◽  
Author(s):  
James A. Popio ◽  
John R. Luchini

Abstract This study compares data from the two Society of Automotive Engineers test methods for rolling resistance: J-2452 (Stepwise Coast-Down) and J-1269 (Equilibrium) steady state. The ability of the two methods to evaluate tires was examined by collecting data for 12 tires. The data were analyzed and the data showed that the two methods ranked the tires the same after the data were regressed and the rolling resistance magnitude was calculated at the Standard Reference Condition. In addition, analysis of the two methods using this matched set of testing provided an opportunity to evaluate each of these test standards against the other. It was observed that each test has merits absent from the other.


1986 ◽  
Vol 51 (11) ◽  
pp. 2481-2488
Author(s):  
Benitto Mayrhofer ◽  
Jana Mayrhoferová ◽  
Lubomír Neužil ◽  
Jaroslav Nývlt

The paper presents a simple model of recrystallization with countercurrent flows of the solution and the crystals being purified. The model assumes steady-state operating conditions, an equilibrium between the outlet streams of each stage, and the same equilibrium temperature and distribution coefficient for all stages. With these assumptions, the model provides the basis for analyzing the variation in the degree of purity as a function of the number of recrystallization stages. The analysis is facilitated by the use of a diagram constructed for the limiting case of perfect removal of the mother liquor from the crystals between the stages.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Lionel Condé ◽  
Yulemi Gonzalez Quesada ◽  
Florence Bonnet-Magnaval ◽  
Rémy Beaujois ◽  
Luc DesGroseillers

AbstractBackgroundStaufen2 (STAU2) is an RNA binding protein involved in the posttranscriptional regulation of gene expression. In neurons, STAU2 is required to maintain the balance between differentiation and proliferation of neural stem cells through asymmetric cell division. However, the importance of controlling STAU2 expression for cell cycle progression is not clear in non-neuronal dividing cells. We recently showed that STAU2 transcription is inhibited in response to DNA-damage due to E2F1 displacement from theSTAU2gene promoter. We now study the regulation of STAU2 steady-state levels in unstressed cells and its consequence for cell proliferation.ResultsCRISPR/Cas9-mediated and RNAi-dependent STAU2 depletion in the non-transformed hTERT-RPE1 cells both facilitate cell proliferation suggesting that STAU2 expression influences pathway(s) linked to cell cycle controls. Such effects are not observed in the CRISPR STAU2-KO cancer HCT116 cells nor in the STAU2-RNAi-depleted HeLa cells. Interestingly, a physiological decrease in the steady-state level of STAU2 is controlled by caspases. This effect of peptidases is counterbalanced by the activity of the CHK1 pathway suggesting that STAU2 partial degradation/stabilization fines tune cell cycle progression in unstressed cells. A large-scale proteomic analysis using STAU2/biotinylase fusion protein identifies known STAU2 interactors involved in RNA translation, localization, splicing, or decay confirming the role of STAU2 in the posttranscriptional regulation of gene expression. In addition, several proteins found in the nucleolus, including proteins of the ribosome biogenesis pathway and of the DNA damage response, are found in close proximity to STAU2. Strikingly, many of these proteins are linked to the kinase CHK1 pathway, reinforcing the link between STAU2 functions and the CHK1 pathway. Indeed, inhibition of the CHK1 pathway for 4 h dissociates STAU2 from proteins involved in translation and RNA metabolism.ConclusionsThese results indicate that STAU2 is involved in pathway(s) that control(s) cell proliferation, likely via mechanisms of posttranscriptional regulation, ribonucleoprotein complex assembly, genome integrity and/or checkpoint controls. The mechanism by which STAU2 regulates cell growth likely involves caspases and the kinase CHK1 pathway.


1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous

The mechanism whereby gastrin-type receptor and muscarinic M3-type receptor regulate free intracellular Ca2+ concentration ([Ca2+]i) was studied in rabbit gastric parietal cells stimulated by either gastrin or carbachol. Both agonists induced a biphasic [Ca2+]i response: a transient [Ca2+]i rise, followed by a sustained steady state depending on extracellular Ca2+. Gastrin and carbachol also caused a rapid and transient increase in Mn2+ influx (a tracer for bivalent-cation entry). Pre-stimulation of cells with one agonist drastically decreased both [Ca2+]i increase and Mn2+ influx induced by the other. Neither diltiazem nor pertussistoxin treatment had any effect on agonist-stimulated Mn2+ entry. Thapsigargin, a Ca(2+)-pump inhibitor, induced a biphasic [Ca2+]i increase, and enhanced the rate of Mn2+ entry. Preincubation of cells with thapsigargin inhibits the [Ca2+]i increase as well as Mn2+ entry stimulated by gastrin or by carbachol. Thapsigargin induced a weak but significant increase in Ins(1,4,5)P3 content, but this agent had no effect on the agonist-evoked Ins(1,4,5)P3 response. In permeabilized parietal cells, Ins(1,4,5)P3 and caffeine caused an immediate Ca2+ release from intracellular pools, followed by a reloading of Ca2+ pools which can be prevented in the presence of thapsigargin. We conclude that (i) gastrin and carbachol mobilize common Ca2+ intracellular stores, (ii) Ca2+ permeability secondary to receptor activation involves neither a voltage-sensitive Ca2+ channel nor a GTP-binding protein from the G1 family, and (iii) agonists regulate common Ca2+ channels in depleting intracellular Ca2+ stores.


Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 67-77 ◽  
Author(s):  
A Parket ◽  
O Inbar ◽  
M Kupiec

Abstract The Ty retrotransposons are the main family of dispersed repeated sequences in the yeast Saccharomyces cerevisiae. These elements are flanked by a pair of long terminal direct repeats (LTRs). Previous experiments have shown that Ty elements recombine at low frequencies, despite the fact that they are present in 30 copies per genome. This frequency is not highly increased by treatments that cause DNA damage, such as UV irradiation. In this study, we show that it is possible to increase the recombination level of a genetically marked Ty by creating a double-strand break in it. This break is repaired by two competing mechanisms: one of them leaves a single LTR in place of the Ty, and the other is a gene conversion event in which the marked Ty is replaced by an ectopically located one. In a strain in which the marked Ty has only one LTR, the double-strand break is repaired by conversion. We have also measured the efficiency of repair and monitored the progression of the cells through the cell-cycle. We found that in the presence of a double-strand break in the marked Ty, a proportion of the cells is unable to resume growth.


Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 661
Author(s):  
Hanna Isaksson ◽  
Peter L. Conlin ◽  
Ben Kerr ◽  
William C. Ratcliff ◽  
Eric Libby

Early multicellular organisms must gain adaptations to outcompete their unicellular ancestors, as well as other multicellular lineages. The tempo and mode of multicellular adaptation is influenced by many factors including the traits of individual cells. We consider how a fundamental aspect of cells, whether they reproduce via binary fission or budding, can affect the rate of adaptation in primitive multicellularity. We use mathematical models to study the spread of beneficial, growth rate mutations in unicellular populations and populations of multicellular filaments reproducing via binary fission or budding. Comparing populations once they reach carrying capacity, we find that the spread of mutations in multicellular budding populations is qualitatively distinct from the other populations and in general slower. Since budding and binary fission distribute age-accumulated damage differently, we consider the effects of cellular senescence. When growth rate decreases with cell age, we find that beneficial mutations can spread significantly faster in a multicellular budding population than its corresponding unicellular population or a population reproducing via binary fission. Our results demonstrate that basic aspects of the cell cycle can give rise to different rates of adaptation in multicellular organisms.


Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 8 ◽  
Author(s):  
Umamaheswari Natarajan ◽  
Thiagarajan Venkatesan ◽  
Vijayaraghavan Radhakrishnan ◽  
Shila Samuel ◽  
Appu Rathinavelu

Gene expression is often altered by epigenetic modifications that can significantly influence the growth ability and progression of cancers. SAHA (Suberoylanilide hydroxamic acid, also known as Vorinostat), a well-known Histone deacetylase (HDAC) inhibitor, can stop cancer growth and metastatic processes through epigenetic alterations. On the other hand, Letrozole is an aromatase inhibitor that can elicit strong anti-cancer effects on breast cancer through direct and indirect mechanisms. A newly developed inhibitor, RG7388 specific for an oncogene-derived protein called MDM2, is in clinical trials for the treatment of various cancers. In this paper, we performed assays to measure the effects of cell cycle arrest resulting from individual drug treatments or combination treatments with SAHA + letrozole and SAHA + RG7388, using the MCF-7 breast cancer cells. When SAHA was used individually, or in combination treatments with RG7388, a significant increase in the cytotoxic effect was obtained. Induction of cell cycle arrest by SAHA in cancer cells was evidenced by elevated p21 protein levels. In addition, SAHA treatment in MCF-7 cells showed significant up-regulation in phospho-RIP3 and MLKL levels. Our results confirmed that cell death caused by SAHA treatment was primarily through the induction of necroptosis. On the other hand, the RG7388 treatment was able to induce apoptosis by elevating BAX levels. It appears that, during combination treatments, with SAHA and RG7388, two parallel pathways might be induced simultaneously, that could lead to increased cancer cell death. SAHA appears to induce cell necroptosis in a p21-dependent manner, and RG7388 seems to induce apoptosis in a p21-independent manner, outlining differential mechanisms of cell death induction. However, further studies are needed to fully understand the intracellular mechanisms that are triggered by these two anti-cancer agents.


Sign in / Sign up

Export Citation Format

Share Document