scholarly journals A nucleostemin-like GTPase required for normal apical and floral meristem development in Arabidopsis

2012 ◽  
Vol 23 (8) ◽  
pp. 1446-1456 ◽  
Author(s):  
Xiaomin Wang ◽  
Daniel K. Gingrich ◽  
Yunfei Deng ◽  
Zonglie Hong
Keyword(s):  
Flower Development ◽  
Cell Cycle Progression ◽  
Floral Organ ◽  
Regulatory Proteins ◽  
Cycle Progression ◽  
New Class ◽  
Meristem Development ◽  
Promote Cell Cycle Progression ◽  
Floral Primordia ◽  
Floral Organ Specification

Mammalian nucleostemin (NS) is preferentially expressed in stem cells and acts to promote cell cycle progression. In plants, stem cell activities have to be terminated during flower development, and this process requires the activation of AGAMOUS (AG) gene expression. Here, a nucleostemin-like 1 gene, NSN1, is shown to be required for flower development in Arabidopsis. The NSN1 mRNA was found in the inflorescence meristem and floral primordia, and its protein was localized to the nucleoli. Both heterozygous and homozygous plants developed defective flowers on inflorescences that were eventually terminated by the formation of carpelloid flowers. Overexpression of NSN1 resulted in loss of apical dominance and formation of defective flowers. Expression of the AG gene was found to be up-regulated in nsn1. The carpelloid flower defect of nsn1 was suppressed by the ag mutation in the nsn1 ag double mutant, whereas double mutants of nsn1 apetala2 (ap2) displayed enhanced defective floral phenotypes. These results suggest that in the delicately balanced regulatory network, NSN1 acts to repress AG and plays an additive role with AP2 in floral organ specification. As a midsize nucleolar GTPase, NSN1 represents a new class of regulatory proteins required for flower development in Arabidopsis.

scholarly journals Targeting RB1 Loss in Cancers

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3737
Author(s):  
Paing Linn ◽  
Susumu Kohno ◽  
Jindan Sheng ◽  
Nilakshi Kulathunga ◽  
Hai Yu ◽  
...  
Keyword(s):  
Cell Cycle Progression ◽  
Suppressor Gene ◽  
Therapeutic Approaches ◽  
Neighboring Gene ◽  
Genomic Aberration ◽  
Cycle Progression ◽  
Synthetic Lethal ◽  
Mitotic Kinases ◽  
Promote Cell Cycle Progression ◽  
Almost All

Retinoblastoma protein 1 (RB1) is encoded by a tumor suppressor gene that was discovered more than 30 years ago. Almost all mitogenic signals promote cell cycle progression by braking on the function of RB1 protein through mono- and subsequent hyper-phosphorylation mediated by cyclin-CDK complexes. The loss of RB1 function drives tumorigenesis in limited types of malignancies including retinoblastoma and small cell lung cancer. In a majority of human cancers, RB1 function is suppressed during tumor progression through various mechanisms. The latter gives rise to the acquisition of various phenotypes that confer malignant progression. The RB1-targeted molecules involved in such phenotypic changes are good quarries for cancer therapy. Indeed, a variety of novel therapies have been proposed to target RB1 loss. In particular, the inhibition of a number of mitotic kinases appeared to be synthetic lethal with RB1 deficiency. A recent study focusing on a neighboring gene that is often collaterally deleted together with RB1 revealed a pharmacologically targetable vulnerability in RB1-deficient cancers. Here we summarize current understanding on possible therapeutic approaches targeting functional or genomic aberration of RB1 in cancers.

scholarly journals PARP14 regulates cyclin D1 expression to promote cell-cycle progression

Oncogene ◽  
2021 ◽  
Author(s):  
Michael J. O’Connor ◽  
Tanay Thakar ◽  
Claudia M. Nicolae ◽  
George-Lucian Moldovan
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Promote Cell Cycle Progression

scholarly journals Akt/Protein Kinase B-Dependent Phosphorylation and Inactivation of WEE1Hu Promote Cell Cycle Progression at G2/M Transition

2005 ◽  
Vol 25 (13) ◽  
pp. 5725-5737 ◽  
Author(s):  
Kazuhiro Katayama ◽  
Naoya Fujita ◽  
Takashi Tsuruo
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Kinase Inhibitor ◽  
Phosphorylation Site ◽  
Cytoplasmic Localization ◽  
M Cell ◽  
Serine Threonine Kinase ◽  
Cycle Progression ◽  
M Phase ◽  
Promote Cell Cycle Progression

ABSTRACT The serine/threonine kinase Akt is known to promote cell growth by regulating the cell cycle in G1 phase through activation of cyclin/Cdk kinases and inactivation of Cdk inhibitors. However, how the G2/M phase is regulated by Akt remains unclear. Here, we show that Akt counteracts the function of WEE1Hu. Inactivation of Akt by chemotherapeutic drugs or the phosphatidylinositide-3-OH kinase inhibitor LY294002 induced G2/M arrest together with the inhibitory phosphorylation of Cdc2. Because the increased Cdc2 phosphorylation was completely suppressed by wee1hu gene silencing, WEE1Hu was associated with G2/M arrest induced by Akt inactivation. Further analyses revealed that Akt directly bound to and phosphorylated WEE1Hu during the S to G2 phase. Serine-642 was identified as an Akt-dependent phosphorylation site. WEE1Hu kinase activity was not affected by serine-642 phosphorylation. We revealed that serine-642 phosphorylation promoted cytoplasmic localization of WEE1Hu. The nuclear-to-cytoplasmic translocation was mediated by phosphorylation-dependent WEE1Hu binding to 14-3-3θ but not 14-3-3β or -σ. These results indicate that Akt promotes G2/M cell cycle progression by inducing phosphorylation-dependent 14-3-3θ binding and cytoplasmic localization of WEE1Hu.

scholarly journals In silico APC/C substrate discovery reveals cell cycle degradation of chromatin regulators including UHRF1

2020 ◽  
Author(s):  
Jennifer L. Kernan ◽  
Raquel C. Martinez-Chacin ◽  
Xianxi Wang ◽  
Rochelle L. Tiedemann ◽  
Thomas Bonacci ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Methylation ◽  
In Silico ◽  
Cell Cycle Progression ◽  
Vital Role ◽  
Regulatory Proteins ◽  
Phase Cell ◽  
Cell Physiology ◽  
Cycle Progression ◽  
Chromatin Regulator

AbstractThe Anaphase-Promoting Complex/Cyclosome (APC/C) is an E3 ubiquitin ligase and critical regulator of cell cycle progression. Despite its vital role, it has remained challenging to globally map APC/C substrates. By combining orthogonal features of known substrates, we predicted APC/C substrates in silico. This analysis identified many known substrates and suggested numerous candidates. Unexpectedly, chromatin regulatory proteins are enriched among putative substrates and we show that several chromatin proteins bind APC/C, oscillate during the cell cycle and are degraded following APC/C activation, consistent with being direct APC/C substrates. Additional analysis revealed detailed mechanisms of ubiquitylation for UHRF1, a key chromatin regulator involved in histone ubiquitylation and DNA methylation maintenance. Disrupting UHRF1 degradation at mitotic exit accelerates G1-phase cell cycle progression and perturbs global DNA methylation patterning in the genome. We conclude that APC/C coordinates crosstalk between cell cycle and chromatin regulatory proteins. This has potential consequences in normal cell physiology, where the chromatin environment changes depending on proliferative state, as well as in disease.

scholarly journals Control of flower development in Arabidopsis thaliana by APETALA1 and interacting genes

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 721-743 ◽  
Author(s):  
J. L. Bowman ◽  
J. Alvarez ◽  
D. Weigel ◽  
E. M. Meyerowitz ◽  
D. R. Smyth
Keyword(s):  
Arabidopsis Thaliana ◽  
In Situ Hybridization ◽  
Flower Development ◽  
Floral Organ ◽  
Allelic Series ◽  
Flower Meristem ◽  
Petal Development ◽  
Two Phases ◽  
Floral Organ Specification

Mutations in the APETALA1 gene disturb two phases of flower development, flower meristem specification and floral organ specification. These effects become manifest as a partial conversion of flowers into inflorescence shoots and a disruption of sepal and petal development. We describe the changes in an allelic series of nine apetala1 mutants and show that the two functions of APETALA1 are separable. We have also studied the interaction between APETALA1 and other floral genes by examining the phenotypes of multiply mutant plants and by in situ hybridization using probes for several floral control genes. The results suggest that the products of APETALA1 and another gene, LEAFY, are required to ensure that primordia arising on the flanks of the inflorescence apex adopt a floral fate, as opposed to becoming an inflorescence shoot. APETALA1 and LEAFY have distinct as well as overlapping functions and they appear to reinforce each other's action. CAULIFLOWER is a newly discovered gene which positively regulates both APETALA1 and LEAFY expression. All functions of CAULIFLOWER are redundant with those of APETALA1. APETALA2 also has an early function in reinforcing the action of APETALA1 and LEAFY, especially if the activity of either is compromised by mutation. After the identity of a flower primordium is specified, APETALA1 interacts with APETALA2 in controlling the development of the outer two whorls of floral organs.

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