scholarly journals The Botrytis cinerea PAK kinase BcCla4 mediates morphogenesis, growth and cell cycle regulating processes downstream of BcRac

2017 ◽  
Vol 104 (3) ◽  
pp. 487-498 ◽  
Author(s):  
Anna Minz-Dub ◽  
Amir Sharon
Keyword(s):  
Cell Cycle ◽  
Botrytis Cinerea ◽  
Pak Kinase

scholarly journals Cytokinin regulates energy utilization in Botrytis cinerea

2021 ◽  
Author(s):  
Gautam Anand ◽  
Rupali Gupta ◽  
Maya Bar
Keyword(s):  
Cell Cycle ◽  
Energy Consumption ◽  
Growth Inhibition ◽  
Botrytis Cinerea ◽  
Nutrient Availability ◽  
Energy Utilization ◽  
Metabolic Effects ◽  
Cellular Trafficking ◽  
Cytoskeleton Organization

AbstractThe plant hormone cytokinin (CK) is an important developmental regulator, promoting morphogenesis and delaying senescence. Previous work by us and others has demonstrated that CKs also mediate plant immunity and disease resistance. Some phytopathogens have been reported to secrete CKs, and may manipulate CK signaling to regulate the host cell cycle and nutrient allocation, to improve their pathogenic abilities. In a recent work, we demonstrated that CK directly inhibits the growth, development, and virulence of fungal phytopathogens, by down regulating the cell cycle and reducing cytoskeleton organization and cellular trafficking in the fungus. Here, focusing on Botrytis cinerea (Bc), we report that the effect of CK on Bc is tied to nutrient availability; CK strongly inhibits Bc growth and de-regulated cytoskeleton organization in a nutrient rich environment, but has a diminished effect when nutrients are scarce. Using biochemical assays and transgenic redox sensitive botrytis lines, we examined the effect of CK on energy consumption in the fungus, and demonstrate that CK promotes glycolysis and energy consumption in Bc, both in vitro and in planta. Here, glycolysis and increased oxidation were stronger with waning nutrient availability. Transcriptomic data further supports our findings, demonstrating significant upregulation to glycolysis, oxidative phosphorylation, and sucrose metabolism, upon CK treatment. The metabolic effects of CK on the fungus likely reflect the role of plant CK during early infection by necrotrophic pathogens, which are known to have an initial, short biotrophic phase. In addition to the plant producing CK during its interaction with the pathogen for defense priming and pathogen inhibition, the pathogen may take advantage of this increased CK to boost its metabolism and energy production, in preparation for the necrotrophic phase of the infection. Thus, the role of CK in controlling senescence can be exploited by diverse phytopathogens to their advantage.Author summaryCytokinin (CK) is one of the primary plant developmental hormones, regulating many developmental processes. Several works have highlighted the involvement of CK in plant defense. We recently reported that CK can directly inhibit fungal plant pathogens. CK inhibits Botrytis cinerea growth by arresting the cell cycle and de-regulating cytoskeleton organization and cellular trafficking. Here, we report that CK positively regulates B. cinerea energy consumption, causing an increase in glycolytic rates and energy consumption. The effect of CK on B. cinerea was dependent on nutrient availability, with CK causing stronger increases in glycolysis and lower growth inhibition when nutrient availably was low, and weaker glycolytic increases coupled with stronger growth inhibition in a high nutrient environment. We propose that CK can be viewed as a bidirectional signaling molecule in plant pathogen interactions: CK acts as a signal to the fungus that plant tissue is present, causing it to activate sugar and energy metabolism pathways to take advantage of the available food source, while at the same time, CK is employed by the plant to inhibit the attacking pathogen.

scholarly journals Involvement of Botrytis cinerea Small GTPases BcRAS1 and BcRAC in Differentiation, Virulence, and the Cell Cycle

2013 ◽  
Vol 12 (12) ◽  
pp. 1609-1618 ◽  
Author(s):  
Anna Minz Dub ◽  
Leonie Kokkelink ◽  
Bettina Tudzynski ◽  
Paul Tudzynski ◽  
Amir Sharon
Keyword(s):  
Cell Cycle ◽  
Botrytis Cinerea ◽  
Cell Cycle Progression ◽  
Mapk Signaling ◽  
Small Gtpases ◽  
Mitogen Activated Protein Kinase ◽  
Polar Growth ◽  
Content Type ◽  
Mold Fungus ◽  
Actin Localization

ABSTRACTSmall GTPases of the Ras superfamily are highly conserved proteins that are involved in various cellular processes, in particular morphogenesis, differentiation, and polar growth. Here we report on the analysis of RAS1 and RAC homologues from the gray mold fungusBotrytis cinerea. We show that these small GTPases are individually necessary for polar growth, reproduction, and pathogenicity, required for cell cycle progression through mitosis (BcRAC), and may lie upstream of the stress-related mitogen-activated protein kinase (MAPK) signaling pathway.bcras1andbcracdeletion strains had reduced growth rates, and their hyphae were hyperbranched and deformed. In addition, both strains were vegetatively sterile and nonpathogenic. A strain expressing a constitutively active (CA) allele of the BcRAC protein had partially similar but milder phenotypes. Similar to the deletion strains, the CA-BcRAC strain did not produce any conidia and had swollen hyphae. In contrast to the two deletion strains, however, the growth rate of the CA-BcRAC strain was normal, and it caused delayed but well-developed disease symptoms. Microscopic examination revealed an increased number of nuclei and disturbance of actin localization in the CA-BcRAC strain. Further work with cell cycle- and RAC-specific inhibitory compounds associated the BcRAC protein with progression of the cell cycle through mitosis, possibly via an effect on microtubules. Together, these results show that the multinucleate phenotype of the CA-BcRAC strain could result from at least two defects: disruption of polar growth through disturbed actin localization and uncontrolled nuclear division due to constitutive activity of BcRAC.

Maytansine-Induced Mitotic Arrest in Human Lymphoblasts

1977 ◽  
Vol 35 ◽  
pp. 460-461
Author(s):  
Tai-Te Chao ◽  
John Sullivan ◽  
Awtar Krishan
Keyword(s):  
Electron Microscopy ◽  
Cell Cycle ◽  
Transmission Electron Microscopy ◽  
Tubulin Polymerization ◽  
Vinca Alkaloids ◽  
Antimitotic Activity ◽  
Transmission Electron ◽  
Flow Microfluorometry ◽  
Brain Tubulin

Maytansine, a novel ansa macrolide (1), has potent anti-tumor and antimitotic activity (2, 3). It blocks cell cycle traverse in mitosis with resultant accumulation of metaphase cells (4). Inhibition of brain tubulin polymerization in vitro by maytansine has also been reported (3). The C-mitotic effect of this drug is similar to that of the well known Vinca- alkaloids, vinblastine and vincristine. This study was carried out to examine the effects of maytansine on the cell cycle traverse and the fine struc- I ture of human lymphoblasts.Log-phase cultures of CCRF-CEM human lymphoblasts were exposed to maytansine concentrations from 10-6 M to 10-10 M for 18 hrs. Aliquots of cells were removed for cell cycle analysis by flow microfluorometry (FMF) (5) and also processed for transmission electron microscopy (TEM). FMF analysis of cells treated with 10-8 M maytansine showed a reduction in the number of G1 cells and a corresponding build-up of cells with G2/M DNA content.

Fibronexus-Like Adhesion Sites are Present at the Invasive Zones of Human Epidermoid Carcinomas

1982 ◽  
Vol 40 ◽  
pp. 106-109
Author(s):  
Irwin I. Singer
Keyword(s):  
Cell Cycle ◽  
Serum Concentration ◽  
Substrate Binding ◽  
High Serum ◽  
Adhesion Sites ◽  
Substrate Adhesion ◽  
Focal Contacts ◽  
Adhesion Complex ◽  
Low Serum

Our previous results indicate that two types of fibronectin-cytoskeletal associations may be formed at the fibroblast surface: dorsal matrixbinding fibronexuses generated in high serum (5% FBS) cultures, and ventral substrate-adhering units formed in low serum (0.3% FBS) cultures. The substrate-adhering fibronexus consists of at least vinculin (VN) and actin in its cytoplasmic leg, and fibronectin (FN) as one of its major extracellular components. This substrate-adhesion complex is localized in focal contacts, the sites of closest substratum approach visualized with interference reflection microscopy, which appear to be the major points of cell-tosubstrate adhesion. In fibroblasts, the latter substrate-binding complex is characteristic of cultures that are arrested at the G1 phase of the cell cycle due to the low serum concentration in their medium. These arrested fibroblasts are very well spread, flattened, and immobile.

Immunocytochemical studies on the behavior of RuBisCO and LHCP II during the cell cycle of synchronized Euglena gracilis

1990 ◽  
Vol 48 (3) ◽  
pp. 662-663
Author(s):  
Tetsuaki Osafune ◽  
Shuji Sumida ◽  
Tomoko Ehara ◽  
Eiji Hase ◽  
Jerome A. Schiff
Keyword(s):  
Cell Cycle ◽  
Immunoelectron Microscopy ◽  
Growth Phase ◽  
Euglena Gracilis ◽  
Dark Period ◽  
Light Period ◽  
Carboxylase Activity ◽  
Immunocytochemical Studies ◽  
Lhcp Ii

Changes in the morphology of pyrenoid and the distribution of RuBisCO in the chloroplast of Euglena gracilis were followed by immunoelectron microscopy during the cell cycle in a light (14 h)- dark (10 h) synchronized culture under photoautotrophic conditions. The imrnunoreactive proteins wereconcentrated in the pyrenoid, and less densely distributed in the stroma during the light period (growth phase, Fig. 1-2), but the pyrenoid disappeared during the dark period (division phase), and RuBisCO was dispersed throughout the stroma. Toward the end of the division phase, the pyrenoid began to form in the center of the stroma, and RuBisCO is again concentrated in that pyrenoid region. From a comparison of photosynthetic CO2-fixation with the total carboxylase activity of RuBisCO extracted from Euglena cells in the growth phase, it is suggested that the carboxylase in the pyrenoid functions in CO2-fixation in photosynthesis.

Effect of Chrysanthemum flavonoids on growth and cell cycle regulators of gastric cancer cell

2010 ◽  
Vol 34 (8) ◽  
pp. S50-S50
Author(s):  
Xiaoyan Pan ◽  
Xinmei Zhou ◽  
Guangtao Xu ◽  
Lingfen Miao ◽  
Shuoru Zhu
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cell Cycle Regulators

Repair pathway choice for double-strand breaks

2020 ◽  
Vol 64 (5) ◽  
pp. 765-777 ◽  
Author(s):  
Yixi Xu ◽  
Dongyi Xu
Keyword(s):  
Cell Cycle ◽  
Double Strand Breaks ◽  
Homologous Region ◽  
Gene Repair ◽  
Repair Pathway ◽  
Dna Double Strand Breaks ◽  
Environmental Radiation ◽  
Strand Breaks ◽  
Dna End Resection ◽  
End Resection

Abstract Deoxyribonucleic acid (DNA) is at a constant risk of damage from endogenous substances, environmental radiation, and chemical stressors. DNA double-strand breaks (DSBs) pose a significant threat to genomic integrity and cell survival. There are two major pathways for DSB repair: nonhomologous end-joining (NHEJ) and homologous recombination (HR). The extent of DNA end resection, which determines the length of the 3′ single-stranded DNA (ssDNA) overhang, is the primary factor that determines whether repair is carried out via NHEJ or HR. NHEJ, which does not require a 3′ ssDNA tail, occurs throughout the cell cycle. 53BP1 and the cofactors PTIP or RIF1-shieldin protect the broken DNA end, inhibit long-range end resection and thus promote NHEJ. In contrast, HR mainly occurs during the S/G2 phase and requires DNA end processing to create a 3′ tail that can invade a homologous region, ensuring faithful gene repair. BRCA1 and the cofactors CtIP, EXO1, BLM/DNA2, and the MRE11–RAD50–NBS1 (MRN) complex promote DNA end resection and thus HR. DNA resection is influenced by the cell cycle, the chromatin environment, and the complexity of the DNA end break. Herein, we summarize the key factors involved in repair pathway selection for DSBs and discuss recent related publications.

Gut-enriched kruppel-like factor (GKLF) inhibits cellular proliferation by blocking the G1/S boundary of the cell cycle

2001 ◽  
Vol 120 (5) ◽  
pp. A103-A103
Author(s):  
X CHEN ◽  
D JOHNS ◽  
D GEIMAN ◽  
E MARBAN ◽  
V YANG
Keyword(s):  
Cell Cycle ◽  
Cellular Proliferation
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