an3-Mediated Compensation Is Dependent on a Cell-Autonomous Mechanism in Leaf Epidermal Tissue

2020 ◽  
Vol 61 (6) ◽  
pp. 1181-1190
Author(s):  
Mamoru Nozaki ◽  
Kensuke Kawade ◽  
Gorou Horiguchi ◽  
Hirokazu Tsukaya
Keyword(s):  
Cell Proliferation ◽  
Cell Size ◽  
Leaf Development ◽  
Cell Expansion ◽  
Size Determination ◽  
Wild Type ◽  
Specific Expression ◽  
Autonomous Action ◽  
Epidermal Tissue ◽  
A Cell

Abstract Leaves are formed by coordinated growth of tissue layers driven by cell proliferation and expansion. Compensation, in which a defect in cell proliferation induces compensated cell enlargement (CCE), plays an important role in cell-size determination during leaf development. We previously reported that CCE triggered by the an3 mutation is observed in epidermal and subepidermal layers in Arabidopsis thaliana (Arabidopsis) leaves. Interestingly, CCE is induced in a non-cell autonomous manner between subepidermal cells. However, whether CCE in the subepidermis affects cell size in the adjacent epidermis is still unclear. We induced layer-specific expression of AN3 in an3 leaves and found that CCE in the subepidermis had little impact on cell-size determination in the epidermis, and vice versa, suggesting that CCE is induced in a tissue-autonomous manner. Examination of the epidermis in an3 leaves having AN3-positive and -negative sectors generated by Cre/loxP revealed that, in contrast to the subepidermis, CCE occurred exclusively in AN3-negative epidermal cells, indicating a cell autonomous action of an3-mediated compensation in the epidermis. These results clarified that the epidermal and subepidermal tissue layers have different cell autonomies in CCE. In addition, quantification of cell-expansion kinetics in epidermal and subepidermal tissues of the an3 showed that the tissues exhibited a similar temporal profile to reach a peak cell-expansion rate as compared to wild type. This might be one feature representing that the two tissue layers retain their growth coordination even in the presence of CCE.

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

Growth in cell length in the fission yeast Schizosaccharomyces pombe

1985 ◽  
Vol 75 (1) ◽  
pp. 357-376 ◽  
Author(s):  
J.M. Mitchison ◽  
P. Nurse
Keyword(s):  
Schizosaccharomyces Pombe ◽  
Cell Size ◽  
Single Cells ◽  
Temperature Shift ◽  
Time Lapse ◽  
Cell Length ◽  
Wild Type ◽  
Cycle Growth ◽  
A Cell ◽  
Mutant Cells

The cylindrical cells of Schizosaccharomyces pombe grow in length by extension at the ends and not the middle. At the beginning of the cell cycle, growth is restricted to the ‘old end’, which existed in the previous cycle. Later on, the ‘new end’, formed from the septum, starts to grow at a point in the cycle that we have called NETO (‘new end take-off’). Fluorescence microscopy on cells stained with Calcofluor has been used to study NETO in size mutants, in blocked cdc mutants and with different growth temperatures and media. In wild-type cells (strain 972) NETO happens at 0.34 of the cycle with a cell length of 9.5 microns. With size mutants that are smaller at division, NETO takes place at the same size (9.0-9.5 microns) but this is not achieved until later in the cycle. Another control operates in larger size mutants since NETO occurs at the same stage of the cycle (about 0.32) as in wild type but at a larger cell size. This control is probably a requirement to have completed an event in early G2, since most cdc mutant cells blocked before this point in the cycle do not show NETO whereas most of those blocked in late G2 do show it. We conclude that NETO only happens if: (1) the cell length is greater than a critical value of 9.0-9.5 microns; and (2) the cell has traversed the first 0.3-0.35 of the cycle and passed early G2. NETO is delayed in poor media, in which cell size is also reduced. Temperature has little effect on NETO under steady-state conditions, but there is a transient delay for some hours after a temperature shift. NETO is later in another wild-type strain, 132. Time-lapse photomicrography was used to follow the rates of length growth in single cells. Wild-type cells showed two linear segments during the first 75% of the cycle. There was a rate-change point (RCP), coincident with NETO, where the rate of total length extension increased by 35%. This increase was not due simply to the start of new-end growth, since old-end growth slowed down in some cells at the RCP. cdc 11.123 is a mutant in which septation and division is blocked at 35 degrees C but nuclear division continues.(ABSTRACT TRUNCATED AT 400 WORDS)

Vein density is independent of epidermal cell size in Arabidopsis mutants

2017 ◽  
Vol 44 (4) ◽  
pp. 410 ◽  
Author(s):  
Madeline R. Carins Murphy ◽  
Graham J. Dow ◽  
Gregory J. Jordan ◽  
Timothy J. Brodribb
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Size ◽  
Epidermal Cell ◽  
Cell Expansion ◽  
Vascular Plants ◽  
Cost Ratio ◽  
Wild Type ◽  
Vein Density ◽  
Leaf Tissues ◽  
Epidermal Cell Size

Densities of leaf minor veins and stomata are co-ordinated within and across vascular plants. This maximises the benefit-to-cost ratio of leaf construction by ensuring stomata receive the minimum amount of water required to maintain optimal aperture. A ‘passive dilution’ mechanism in which densities of veins and stomata are co-regulated by epidermal cell size is thought to facilitate this co-ordination. However, unlike stomata, veins are spatially isolated from the epidermis and thus may not be directly regulated by epidermal cell expansion. Here, we use mutant genotypes of Arabidopsis thaliana (L.) Heynh. with altered stomatal and epidermal cell development to test this mechanism. To do this we compared observed relationships between vein density and epidermal cell size with modelled relationships that assume veins and stomata are passively diluted by epidermal cell expansion. Data from wild-type plants were consistent with the ‘passive dilution’ mechanism, but in mutant genotypes vein density was independent of epidermal cell size. Hence, vein density is not causally linked to epidermal cell expansion. This suggests that adaptation favours synchronised changes to the cell size of different leaf tissues to coordinate veins and stomata, and thus balance water supply with transpirational demand.

scholarly journals Role of α1-adrenoceptor subtypes on corneal epithelial thickness and cell proliferation in mice

2018 ◽  
Vol 315 (5) ◽  
pp. C757-C765 ◽  
Author(s):  
Aytan Musayeva ◽  
Caroline Manicam ◽  
Andreas Steege ◽  
Christoph Brochhausen ◽  
Beate K. Straub ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Cell Size ◽  
Corneal Epithelium ◽  
Messenger Rna ◽  
Rank Order ◽  
Wild Type ◽  
Corneal Epithelial ◽  
Epithelial Thickness ◽  
Corneal Epithelial Thickness

Adrenergic stimuli are important for corneal epithelial structure and healing. The purpose of the present study was to examine the hypothesis that the lack of a single α1-adrenoceptor (α1-AR) subtype affects corneal epithelial thickness and cell proliferation. Expression levels of α1-AR mRNA were determined in mouse cornea using real-time PCR. In mice devoid of one of the three α1-AR subtypes (α1A-AR−/−, α1B-AR−/−, α1D-AR−/−) and in wild-type controls, thickness of individual corneal layers, the number of epithelial cell layers, and average epithelial cell size were determined in cryosections. Endothelial cell density and morphology were calculated in corneal explants, and epithelial cell proliferation rate was determined with immunofluorescence microscopy. Moreover, the ultrastructure of the corneal epithelium was examined by transmission electron microscopy. Messenger RNA for all three α1-AR subtypes was expressed in whole cornea and in corneal epithelium from wild-type mice with a rank order of abundance of α1A ≥ α1B > α1D. In contrast, no α1-AR mRNA was detected in the stroma, and only α1B-AR mRNA was found in the Descemet endothelial complex. Remarkably, corneal epithelial thickness and mean epithelial cell size were reduced in α1A-AR−/− mice. Our findings suggest that the α1A-AR exerts growth effects in mouse corneal epithelial cells.

scholarly journals A cell sizer network involving Cln3 and Far1 controls entrance into S phase in the mitotic cycle of budding yeast

2004 ◽  
Vol 167 (3) ◽  
pp. 433-443 ◽  
Author(s):  
Lilia Alberghina ◽  
Riccardo L. Rossi ◽  
Lorenzo Querin ◽  
Valeria Wanke ◽  
Marco Vanoni
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Replication ◽  
Carbon Source ◽  
Protein Content ◽  
Cell Size ◽  
Mitotic Cycle ◽  
S Phase ◽  
Wild Type ◽  
Bud Emergence ◽  
A Cell

Saccharomyces cerevisiae must reach a carbon source-modulated critical cell size, protein content per cell at the onset of DNA replication (Ps), in order to enter S phase. Cells grown in glucose are larger than cells grown in ethanol. Here, we show that an increased level of the cyclin-dependent inhibitor Far1 increases cell size, whereas far1Δ cells start bud emergence and DNA replication at a smaller size than wild type. Cln3Δ, far1Δ, and strains overexpressing Far1 do not delay budding during an ethanol glucose shift-up as wild type does. Together, these findings indicate that Cln3 has to overcome Far1 to trigger Cln–Cdc28 activation, which then turns on SBF- and MBF-dependent transcription. We show that a second threshold is required together with the Cln3/Far1 threshold for carbon source modulation of Ps. A new molecular network accounting for the setting of Ps is proposed.

scholarly journals Perturbation of GABA Biosynthesis Links Cell Cycle to Control Arabidopsis thaliana Leaf Development

2020 ◽  
Author(s):  
Yaxin Gong ◽  
Han Yue ◽  
Yu Xiang ◽  
Guanghui Yu
Keyword(s):  
Reactive Oxygen Species ◽  
Leaf Development ◽  
Cell Expansion ◽  
Leaf Blade ◽  
Aminobutyric Acid ◽  
Oxygen Species ◽  
Gaba Level ◽  
Wild Type ◽  
Blade Area ◽  
In The Wild

AbstractTo investigate the molecular mechanism underlying increasing leaf area in γ-Aminobutyric acid (GABA) biosynthetic mutants, the first pair of true leaves of GABA biosynthetic mutants was measured. The results showed that the leaf blade area in GABA biosynthetic mutants was larger than that of the wild type to different extents, and the area of the leaf epidermal cells in mutants was larger than that of the wild type. DNA polyploid analysis showed that polyploid cells in GABA biosynthetic mutants were appearing earlier and more abundant than in the wild type. To check the correlation between cell size and endoreplication, the expression of factors involving endocycles, including D-type cyclin gene (CYCD3;1, CYCD3;2, CYCD3;3, and CYCD4;1) and kinase CKDA;1, were analysed by qRT-PCR. The results showed that CKDA;1 in GABA biosynthetic mutants was downregulated, and four types of CYCDs showed different expression patterns in different GABA biosynthetic mutants. Inconsistent with this result, for CCS52A (CELL CYCLE SWITCH 52A) (controlling the endocycle entry) in gad2 and gad1/gad2 mutants, the expression of CCS52A2 was significantly higher than that in the wild type. The expression of SIM (SIAMESE) and SMR (SIAMESE-RELATED), which inhibit kinase activity, were also upregulated compared with the control. To further study the possible potential relationship between GABA metabolism and endoreplication, we analysed the reactive oxygen species (ROS) levels in guard cells using ROS fluorescent probes. ROS levels were significantly higher in GABA biosynthetic mutants than the control. All results indicated that cyclin, the cyclin-dependent kinase, and its inhibitory protein were coordinated to participate in endoreplication control at the transcription level in the leaves of GABA biosynthetic mutant Arabidopsis.Contribution to the field statementγ-Aminobutyric acid (GABA) metabolic pathway plays a dual role in plant development. This research investigated the perturbation of GABA biosynthesis on Arabidopsis leave endoreplication for the first time. In the GABA biosynthetic mutants, many genes, participating in cell division regulation, are coordinately transcriptionally expressed to trigger the onset and maintenance of endoreplication, and this led to the cell expansion and the increase leaf blade area. However, this initiation of endoreplication links with the decrease of endogenous GABA level and the increase Reactive oxygen species (ROS). This may be a compensation mechanism to adapt to abnormal GABA level in plant leaf development. Present evidence provided hypothesized that the normal GABA level in plant leaf development plays a brake to inhibit the immature cell expansion and differentiation, and this negative regulation functions a guarantee mechanism to watchdog the normal leaf development. In all, this contribution provides an updated perspective on the role of GABA in plant development.

scholarly journals Molecular networks regulating cell division during Arabidopsis leaf growth

2019 ◽  
Vol 71 (8) ◽  
pp. 2365-2378 ◽  
Author(s):  
Jasmien Vercruysse ◽  
Alexandra Baekelandt ◽  
Nathalie Gonzalez ◽  
Dirk Inzé
Keyword(s):  
Cell Proliferation ◽  
Leaf Development ◽  
Cell Expansion ◽  
Leaf Growth ◽  
Leaf Size ◽  
Mitotic Cell ◽  
Cell Number ◽  
Molecular Networks ◽  
Regulatory Modules ◽  
Increase Cell Number

Abstract Leaves are the primary organs for photosynthesis, and as such have a pivotal role for plant growth and development. Leaf development is a multifactorial and dynamic process involving many genes that regulate size, shape, and differentiation. The processes that mainly drive leaf development are cell proliferation and cell expansion, and numerous genes have been identified that, when ectopically expressed or down-regulated, increase cell number and/or cell size during leaf growth. Many of the genes regulating cell proliferation are functionally interconnected and can be grouped into regulatory modules. Here, we review our current understanding of six important gene regulatory modules affecting cell proliferation during Arabidopsis leaf growth: ubiquitin receptor DA1–ENHANCER OF DA1 (EOD1), GROWTH REGULATING FACTOR (GRF)–GRF-INTERACTING FACTOR (GIF), SWITCH/SUCROSE NON-FERMENTING (SWI/SNF), gibberellin (GA)–DELLA, KLU, and PEAPOD (PPD). Furthermore, we discuss how post-mitotic cell expansion and these six modules regulating cell proliferation make up the final leaf size.

scholarly journals The puc1 Cyclin Regulates the G1 Phase of the Fission Yeast Cell Cycle in Response to Cell Size

2000 ◽  
Vol 11 (2) ◽  
pp. 543-554 ◽  
Author(s):  
Cristina Martı́n-Castellanos ◽  
Miguel A. Blanco ◽  
José M. de Prada ◽  
Sergio Moreno
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Cell Size ◽  
Yeast Cells ◽  
G1 Phase ◽  
Close Relative ◽  
Cell Cycle Distribution ◽  
Cdk Inhibitor ◽  
Wild Type ◽  
A Cell

Eukaryotic cells coordinate cell size with cell division by regulating the length of the G1 and G2 phases of the cell cycle. In fission yeast, the length of the G1 phase depends on a precise balance between levels of positive (cig1, cig2, puc1, and cdc13 cyclins) and negative (rum1 and ste9-APC) regulators of cdc2. Early in G1, cyclin proteolysis and rum1 inhibition keep the cdc2/cyclin complexes inactive. At the end of G1, the balance is reversed and cdc2/cyclin activity down-regulates both rum1 and the cyclin-degrading activity of the APC. Here we present data showing that the puc1 cyclin, a close relative of the Cln cyclins in budding yeast, plays an important role in regulating the length of G1. Fission yeast cells lacking cig1 and cig2 have a cell cycle distribution similar to that of wild-type cells, with a short G1 and a long G2. However, when thepuc1 + gene is deleted in this genetic background, the length of G1 is extended and these cells undergo S phase with a greater cell size than wild-type cells. This G1 delay is completely abolished in cells lacking rum1. Cdc2/puc1 function may be important to down-regulate the rum1 Cdk inhibitor at the end of G1.

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