scholarly journals Auxin Binding by SKP2A Activates Proteolysis of Downstream Cell Cycle Regulators and Promotes Cell Division

2010 ◽  
Vol 22 (12) ◽  
pp. 3877-3877 ◽  
Author(s):  
Jennifer Mach
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Regulators ◽  
Auxin Binding

scholarly journals Molecular Analysis of Fruit Size Regulation in Apple

HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 868C-868
Author(s):  
Anish Malladi* ◽  
Peter Hirst
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Size ◽  
Fruit Size ◽  
Cell Number ◽  
Size Analysis ◽  
Cell Cycle Gene ◽  
Cell Cycle Regulators ◽  
Size Regulation ◽  
Molecular Aspects

Fruit size is a commercially valuable trait. Although several factors are known to affect fruit size in apple, insights into the molecular aspects of its regulation are lacking. Our research aims to understand fruit size regulation using a combination of approaches. Analysis of a large fruited mutant of `Gala', `Grand Gala' (GG), showed that it was 40% heavier than `Gala' at harvest. Increase in size of GG fruit was caused by an increase in the cell size apparent at full bloom. Flow cytometry revealed the presence of multiple levels of ploidy (up to 16C) in GG during early fruit development. Increase in ploidy of GG is hypothesized to be due to endoreduplication, a process normally absent in apple. Endoreduplication is a modification of the cell cycle where DNA replication is not followed by cell division, resulting in increased DNA content accompanied by increased cell size. To understand if the cell cycle is altered in GG, four key cell cycle regulators, MdCDKA1, MdCDKB1, MdCYCB2 and MdCYCD3 have been partially cloned from apple using RT-PCR and RACE. As cell number at the end of the cell division phase is correlated with fruit size at harvest, expression analysis of these genes can provide valuable insights into their role in the regulation of cell number and fruit size. Analysis of cell cycle gene expression in GG may provide key insights into the altered molecular regulation that leads to endoreduplication in the mutant. Parallel approaches being employed to study whether environmental and cultural factors regulate fruit size through an influence on the cell cycle will also be discussed.

scholarly journals dally, a Drosophila member of the glypican family of integral membrane proteoglycans, affects cell cycle progression and morphogenesis via a Cyclin A-mediated process

2002 ◽  
Vol 115 (1) ◽  
pp. 123-130 ◽  
Author(s):  
Hiroshi Nakato ◽  
Bethany Fox ◽  
Scott B. Selleck
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Optic Lobe ◽  
Cyclin A ◽  
Cell Cycle Regulators ◽  
Late Prophase ◽  
Cycle Progression ◽  
Dividing Cells ◽  
Morphological Defects

division abnormally delayed (dally) encodes an integral membrane proteoglycan of the glypican family that affects a number of patterning events during both embryonic and larval development. Earlier studies demonstrated that Dally regulates cellular responses to Wingless (Wg) and Decapentaplegic (Dpp) in a tissue-specific manner, consistent with its proposed role as a growth factor co-receptor. dally mutants also display cell cycle progression defects in specific sets of dividing cells in the developing optic lobe and retina. The affected cells in the retina and lamina show delays in completion of the G2-M segment of the cell cycle. We have investigated the molecular basis of dally-mediated cell division defects by examining the genetic interactions between dally and known cell cycle regulators. Reductions in cyclin A but not cyclin B or string expression, suppress dally cell division defects in the optic lobe. cycA mutations also dominantly rescue many dally adult morphological defects including lethality, phenotypes that are unaffected by reducing cycB function. dally mutants show abnormal Cyclin A expression in the dividing cells affected, with appreciable levels of Cyclin A remaining in late prophase and metaphase, stages where Cyclin A is normally absent. Given that Dally is known to regulate the activity of secreted growth factors our findings suggest that extracellular cues influence the degradation of Cyclin A in a manner that controls cell cycle progression and ultimately, cell division patterning.

Organ-specific cell division abnormalities caused by mutation in a general cell cycle regulator inC. elegans

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2155-2165
Author(s):  
Ivana Kostić ◽  
Richard Roy
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Ectopic Expression ◽  
Cell Lineage ◽  
Intestinal Cells ◽  
Specific Cell ◽  
Cell Cycle Regulators ◽  
Loss Of Function ◽  
C Elegans ◽  
Cell Divisions

The precise control of cell division during development is pivotal for morphogenesis and the correct formation of tissues and organs. One important gene family involved in such control is the p21/p27/p57 class of negative cell cycle regulators. Loss of function of the C. elegans p27 homolog, cki-1, causes extra cell divisions in numerous tissues including the hypodermis, the vulva, and the intestine. We have sought to better understand how cell divisions are controlled upstream or in parallel to cki-1 in specific organs during C. elegans development. By taking advantage of the invariant cell lineage of C. elegans, we used an intestinal-specific GFP reporter in a screen to identify mutants that undergo cell division abnormalities in the intestinal lineage. We have isolated a mutant with twice the wild-type complement of intestinal cells, all of which arise during mid-embryogenesis. This mutant, called rr31, is a fully dominant, maternal-effect, gain-of-function mutation in the cdc-25.1 cell cycle phosphatase that sensitizes the intestinal lineage to an extra cell division. We showed that cdc-25.1 acts at the G1/S transition, as ectopic expression of CDC-25.1 caused entry into S phase in intestinal cells. In addition, we showed that the cdc-25.1(gf) requires cyclin E. The extra cell division defect was shown to be restricted to the E lineage and the E fate is necessary and sufficient to sensitize cells to this mutation.

The C. elegans F-box/WD-repeat protein LIN-23 functions to limit cell division during development

Development ◽  
2000 ◽  
Vol 127 (23) ◽  
pp. 5071-5082 ◽  
Author(s):  
E.T. Kipreos ◽  
S.P. Gohel ◽  
E.M. Hedgecock
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Cell Cycle Regulators ◽  
Loss Of Function ◽  
Repeat Protein ◽  
C Elegans ◽  
Blast Cells ◽  
Wd Repeat ◽  
And Function

In multicellular eukaryotes, a complex program of developmental signals regulates cell growth and division by controlling the synthesis, activation and degradation of G(1) cell cycle regulators. Here we describe the lin-23 gene of Caenorhabditis elegans, which is required to restrain cell proliferation in response to developmental cues. In lin-23 null mutants, all postembryonic blast cells undergo extra divisions, creating supernumerary cells that can differentiate and function normally. In contrast to the inability to regulate the extent of blast cell division in lin-23 mutants, the timing of initial cell cycle entry of blast cells is not affected. lin-23 encodes an F-box/WD-repeat protein that is orthologous to the Saccharomyces cerevisiae gene MET30, the Drosophila melanogaster gene slmb and the human gene betaTRCP, all of which function as components of SCF ubiquitin-ligase complexes. Loss of function of the Drosophila slmb gene causes the growth of ectopic appendages in a non-cell autonomous manner. In contrast, lin-23 functions cell autonomously to negatively regulate cell cycle progression, thereby allowing cell cycle exit in response to developmental signals.

scholarly journals The Modular Circuitry of Apicomplexan Cell Division Plasticity

2021 ◽  
Vol 11 ◽  
Author(s):  
Marc-Jan Gubbels ◽  
Isabelle Coppens ◽  
Kourosh Zarringhalam ◽  
Manoj T. Duraisingh ◽  
Klemens Engelberg
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Parasite Species ◽  
Developmental Stages ◽  
Cell Cycle Regulators ◽  
Cycle Progression ◽  
Apicomplexan Parasites ◽  
Secondary Messengers ◽  
Acting In Concert

The close-knit group of apicomplexan parasites displays a wide variety of cell division modes, which differ between parasites as well as between different life stages within a single parasite species. The beginning and endpoint of the asexual replication cycles is a ‘zoite’ harboring the defining apical organelles required for host cell invasion. However, the number of zoites produced per division round varies dramatically and can unfold in several different ways. This plasticity of the cell division cycle originates from a combination of hard-wired developmental programs modulated by environmental triggers. Although the environmental triggers and sensors differ between species and developmental stages, widely conserved secondary messengers mediate the signal transduction pathways. These environmental and genetic input integrate in division-mode specific chromosome organization and chromatin modifications that set the stage for each division mode. Cell cycle progression is conveyed by a smorgasbord of positively and negatively acting transcription factors, often acting in concert with epigenetic reader complexes, that can vary dramatically between species as well as division modes. A unique set of cell cycle regulators with spatially distinct localization patterns insert discrete check points which permit individual control and can uncouple general cell cycle progression from nuclear amplification. Clusters of expressed genes are grouped into four functional modules seen in all division modes: 1. mother cytoskeleton disassembly; 2. DNA replication and segregation (D&S); 3. karyokinesis; 4. zoite assembly. A plug-and-play strategy results in the variety of extant division modes. The timing of mother cytoskeleton disassembly is hard-wired at the species level for asexual division modes: it is either the first step, or it is the last step. In the former scenario zoite assembly occurs at the plasma membrane (external budding), and in the latter scenario zoites are assembled in the cytoplasm (internal budding). The number of times each other module is repeated can vary regardless of this first decision, and defines the modes of cell division: schizogony, binary fission, endodyogeny, endopolygeny.

Physiological Relevance of Cell Cycle Kinases

2011 ◽  
Vol 91 (3) ◽  
pp. 973-1007 ◽  
Author(s):  
Marcos Malumbres
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Human Disease ◽  
Asymmetric Cell Division ◽  
Cell Types ◽  
Mitotic Checkpoint ◽  
Model Organisms ◽  
Cell Cycle Regulators ◽  
Therapeutic Benefits ◽  
Physiological Relevance

The basic biology of the cell division cycle and its control by protein kinases was originally studied through genetic and biochemical studies in yeast and other model organisms. The major regulatory mechanisms identified in this pioneer work are conserved in mammals. However, recent studies in different cell types or genetic models are now providing a new perspective on the function of these major cell cycle regulators in different tissues. Here, we review the physiological relevance of mammalian cell cycle kinases such as cyclin-dependent kinases (Cdks), Aurora and Polo-like kinases, and mitotic checkpoint regulators (Bub1, BubR1, and Mps1) as well as other less-studied enzymes such as Cdc7, Nek proteins, or Mastl and their implications in development, tissue homeostasis, and human disease. Among these functions, the control of self-renewal or asymmetric cell division in stem/progenitor cells and the ability to regenerate injured tissues is a central issue in current research. In addition, many of these proteins play previously unexpected roles in metabolism, cardiovascular function, or neuron biology. The modulation of their enzymatic activity may therefore have multiple therapeutic benefits in human disease.

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
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