scholarly journals Developmentally Controlled Farnesylation Modulates AtNAP1;1 Function in Cell Proliferation and Cell Expansion during Arabidopsis Leaf Development

2006 ◽  
Vol 142 (4) ◽  
pp. 1412-1426 ◽  
Author(s):  
Arnaud Galichet ◽  
Wilhelm Gruissem
Keyword(s):  
Cell Proliferation ◽  
Leaf Development ◽  
Cell Expansion

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 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 Transcriptional control of ROS homeostasis by KUODA1 regulates cell expansion during leaf development

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Dandan Lu ◽  
Ting Wang ◽  
Staffan Persson ◽  
Bernd Mueller-Roeber ◽  
Jos H.M. Schippers
Keyword(s):  
Leaf Development ◽  
Cell Expansion ◽  
Transcriptional Control ◽  
Ros Homeostasis

scholarly journals Replication history of B lymphocytes reveals homeostatic proliferation and extensive antigen-induced B cell expansion

2007 ◽  
Vol 204 (3) ◽  
pp. 645-655 ◽  
Author(s):  
Menno C. van Zelm ◽  
Tomasz Szczepański ◽  
Mirjam van der Burg ◽  
Jacques J.M. van Dongen
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Expansion ◽  
B Lymphocyte ◽  
Somatic Hypermutation ◽  
Homeostatic Proliferation ◽  
History Of ◽  
Lymphocyte Homeostasis

The contribution of proliferation to B lymphocyte homeostasis and antigen responses is largely unknown. We quantified the replication history of mouse and human B lymphocyte subsets by calculating the ratio between genomic coding joints and signal joints on kappa-deleting recombination excision circles (KREC) of the IGK-deleting rearrangement. This approach was validated with in vitro proliferation studies. We demonstrate that naive mature B lymphocytes, but not transitional B lymphocytes, undergo in vivo homeostatic proliferation in the absence of somatic mutations in the periphery. T cell–dependent B cell proliferation was substantially higher and showed higher frequencies of somatic hypermutation than T cell–independent responses, fitting with the robustness and high affinity of T cell–dependent antibody responses. More extensive proliferation and somatic hypermutation in antigen-experienced B lymphocytes from human adults compared to children indicated consecutive responses upon additional antigen exposures. Our combined observations unravel the contribution of proliferation to both B lymphocyte homeostasis and antigen-induced B cell expansion. We propose an important role for both processes in humoral immunity. These new insights will support the understanding of peripheral B cell regeneration after hematopoietic stem cell transplantation or B cell–directed antibody therapy, and the identification of defects in homeostatic or antigen-induced B cell proliferation in patients with common variable immunodeficiency or another antibody deficiency.

Shade avoidance responses are mediated by the ATHB-2 HD-zip protein, a negative regulator of gene expression

Development ◽  
1999 ◽  
Vol 126 (19) ◽  
pp. 4235-4245 ◽  
Author(s):  
C. Steindler ◽  
A. Matteucci ◽  
G. Sessa ◽  
T. Weimar ◽  
M. Ohgishi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Cell Expansion ◽  
Lateral Root ◽  
Vascular System ◽  
Secondary Growth ◽  
Negative Regulator ◽  
Specific Cell ◽  
Shade Avoidance ◽  
Growth Responses

The ATHB-2 gene encoding an homeodomain-leucine zipper protein is rapidly and strongly induced by changes in the ratio of red to far-red light which naturally occur during the daytime under the canopy and induce in many plants the shade avoidance response. Here, we show that elevated ATHB-2 levels inhibit cotyledon expansion by restricting cell elongation in the cotyledon-length and -width direction. We also show that elevated ATHB-2 levels enhance longitudinal cell expansion in the hypocotyl. Interestingly, we found that ATHB-2-induced, as well as shade-induced, elongation of the hypocotyl is dependent on the auxin transport system. In the root and hypocotyl, elevated ATHB-2 levels also inhibit specific cell proliferation such as secondary growth of the vascular system and lateral root formation. Consistent with the key role of auxin in these processes, we found that auxin is able to rescue the ATHB-2 lateral root phenotype. We also show that reduced levels of ATHB-2 result in reciprocal phenotypes. Moreover, we demonstrate that ATHB-2 functions as a negative regulator of gene expression in a transient assay. Remarkably, the expression in transgenic plants of a derivative of ATHB-2 with the same DNA binding specificity but opposite regulatory properties results in a shift in the orientation of hypocotyl cell expansion toward radial expansion, and in an increase in hypocotyl secondary cell proliferation. A model of ATHB-2 function in the regulation of shade-induced growth responses is proposed.

scholarly journals Control of cell proliferation, cell expansion, and leaf size

2006 ◽  
Vol 18 (1) ◽  
pp. 61-68
Author(s):  
Gorou Horiguchi ◽  
Hirokazu Tsukaya
Keyword(s):  
Cell Proliferation ◽  
Cell Expansion ◽  
Leaf Size

scholarly journals A conserved bacterial protein induces pancreatic beta cell expansion during zebrafish development

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Jennifer Hampton Hill ◽  
Eric A Franzosa ◽  
Curtis Huttenhower ◽  
Karen Guillemin
Keyword(s):  
Cell Proliferation ◽  
Cell Expansion ◽  
Bacterial Species ◽  
Pancreatic Beta Cell ◽  
Fecal Microbiota ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Larval Zebrafish ◽  
Low Diversity ◽  
Early Larval Development

Resident microbes play important roles in the development of the gastrointestinal tract, but their influence on other digestive organs is less well explored. Using the gnotobiotic zebrafish, we discovered that the normal expansion of the pancreatic β cell population during early larval development requires the intestinal microbiota and that specific bacterial members can restore normal β cell numbers. These bacteria share a gene that encodes a previously undescribed protein, named herein BefA (β Cell Expansion Factor A), which is sufficient to induce β cell proliferation in developing zebrafish larvae. Homologs of BefA are present in several human-associated bacterial species, and we show that they have conserved capacity to stimulate β cell proliferation in larval zebrafish. Our findings highlight a role for the microbiota in early pancreatic β cell development and suggest a possible basis for the association between low diversity childhood fecal microbiota and increased diabetes risk.

Small Molecule Combination Enhances CD34+/CD38- Cell Proliferation Via Inhibition of Differentiation

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 658-658
Author(s):  
Lan Wang ◽  
Xin Guan ◽  
Huihui Wang ◽  
Bin Shen ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Small Molecules ◽  
Cell Expansion ◽  
Target Genes ◽  
Ex Vivo ◽  
Hematopoietic Stem ◽  
Qpcr Analysis ◽  
Cd34 Cells ◽  
Cells Cultured

Abstract Hematopoietic stem cells (HSCs) have become increasingly attractive for the therapy of various hematological system disorders. The aim of this study is to identify approaches that promote the expansion of HSCs. We present here the identification of a combination of small molecules and cytokines that is effective in retaining high stemness of hematopoietic stem/progenitor cells while promoting cell proliferation by inhibiting differentiation. Firstly, five small-molecule candidates were screened for their individual effects on ex vivo expansion of human peripheral blood CD34+ cells in the presence of selected cytokines. The best compounds at their optimal concentrations were further analyzed in combination, to achieve maximum capacity for stimulating the CD34+CD38- cell expansion ex vivo. The extent of cell expansion and the immunophenotype of expanded cells were assessed through flow cytometry. Additional cell and molecular assays were performed to confirm that the expanded CD34± cells are functionally normal in vitro. Subsequently, the expanded cells were transplanted into sublethally irradiated NOD/SCID mice for the assessment ofhuman cell viability and engraftment potential in vivo. Furthermore, the expression of several genes in the cell proliferation and differentiation pathways was analyzed through qPCR during the process of CD34±cell expansion. Following multiple rounds of screening, an optimal formula (named as "SVC cocktail") was obtained, which consisted of four cytokines (stem cell factor, flt-3 ligand, thrombopoietin and interleukin-6) and three small molecules (Stem Regenin 1, valproic acid and CAY10433). CD34+ cells cultured with SVC cocktail had a purity of 76.2%±7.5% and reached expansion folds of 27.9±4.3 for CD34+/CD38- HSCs on day 7. In contrast, CD34+ cells cultured with the cytokines alone displayed a purity of 27.4%±6.3% and expansion folds of 15.5±2.2 for CD34+/CD38- cells. The groups with small molecules only (plus DMSO, the vehicle), or with basal medium only, showed no surviving cells on day 4. Furthermore, cell cycle analysis indicated that the SVC cocktail-induced CD34+/CD38- cells stayed in a more quiescent state (G0/G1: 75.2%±3.6%; S: 9.2%±2.4%). On the other hand, the cells cultured without the three small molecules had active DNA synthesis (G0/G1: 56.0%±2.0%; S: 31.8%±3.2%), implicating a trend of enhanced cell differentiation in the cytokine alone group. RT-qPCR analysis further demonstrated that the expression of HSC stemness markers CD90, CD133, CD117, ALDH1, Bmi1, HoxB4, GATA-2, Runx1, and CXCR4 were elevated in the SVC cocktail-induced CD34+ cells, but dramatically reduced or barely detectable in the cytokine alone group. In addition, CFU assays for the SVC cocktail group vs the cytokine alone group demonstrated BFU-E of 54.0±4.6 vs 11.7±1.5, CFU-GM of 71.0±2.7 vs 8.3±2.5, CFU-GEMM of 40.7±3.8 vs 5.0±2.0 and CFU-Mk of 6.7±1.5 vs 0.7±0.6, respectively. For the in vivo engraftment in mouse bone marrow, human CD45 rate in the SVC cocktail group was much higher than in the cytokine alone group (21.1%±2.7% vs 0.5%±0.1%); similar group differences were also found in the CD34+ and CD34+CD38- rate (7.7%±1.4% vs 1.6%±1.2% and 6.8%±2.2% vs 1.6%±0.1% respectively), all at 8 weeks post transplantation. Moreover, qPCR analysis of Notch and Wnt signaling pathways for cultured cells on day 7 showed that the expression of Notch target genes (related to high activation of HSC property) was enhanced in the SVC cocktail group compare to the cytokine group (HES5: 9.2±2.3 vs 3.6±1.4 in arbitrary units; HEY1: 6.3±1.9 vs 2.6±1.2; HES1: 3.2±1.3 vs 1.3±0.4; Notch1: 1.4±0.3 vs 1.2±0.3), whereas the expression of Wnt target genes (related to activation of HSC differentiation) was greater in the cytokine alone group than in the SVC cocktail group (CCND1: 10.1±4.3 vs 1.2±0.8; LEF1: 4.3±0.6 vs 2.9±0.2; PPAR D: 3.4±0.3 vs 1.5±0.1; FZD2: 1.8±0.2 vs 1.0±0.1). Taken together, our results show that the new SVC cocktail is able to retain the characteristics of HSCs remarkably well, by enhancing their expansion while inhibiting their differentiation. Mechanistically, it appears that the three small molecules can effectively inhibit the cytokines' pro-differentiation effects on CD34+CD38- cells without affecting the cytokines' ability to stimulate cell proliferation. Disclosures Wang: Biopharmagen Corp.: Employment. Ren:Biopharmagen Corp: Employment. Jiang:Biopharmagen Corp: Consultancy.

Sign in / Sign up

Export Citation Format

Share Document