Cell cycle and cell size regulation during maize seed development: current understanding and challenging questions.

2017 ◽  
pp. 119-133
Author(s):  
P. A. Sabelli
Author(s):  
M. Rosner ◽  
A. Kowalska ◽  
A. Freilinger ◽  
A-R. Prusa ◽  
E. Marton ◽  
...  

2013 ◽  
pp. 343-346 ◽  
Author(s):  
Ákos Sveiczer ◽  
Anna Rácz-Mónus
Keyword(s):  

HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 868C-868
Author(s):  
Anish Malladi* ◽  
Peter Hirst

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.


2016 ◽  
Vol 113 (51) ◽  
pp. E8238-E8246 ◽  
Author(s):  
Lisa Willis ◽  
Yassin Refahi ◽  
Raymond Wightman ◽  
Benoit Landrein ◽  
José Teles ◽  
...  

Cell size and growth kinetics are fundamental cellular properties with important physiological implications. Classical studies on yeast, and recently on bacteria, have identified rules for cell size regulation in single cells, but in the more complex environment of multicellular tissues, data have been lacking. In this study, to characterize cell size and growth regulation in a multicellular context, we developed a 4D imaging pipeline and applied it to track and quantify epidermal cells over 3–4 d inArabidopsis thalianashoot apical meristems. We found that a cell size checkpoint is not the trigger for G2/M or cytokinesis, refuting the unexamined assumption that meristematic cells trigger cell cycle phases upon reaching a critical size. Our data also rule out models in which cells undergo G2/M at a fixed time after birth, or by adding a critical size increment between G2/M transitions. Rather, cell size regulation was intermediate between the critical size and critical increment paradigms, meaning that cell size fluctuations decay by ∼75% in one generation compared with 100% (critical size) and 50% (critical increment). Notably, this behavior was independent of local cell–cell contact topologies and of position within the tissue. Cells grew exponentially throughout the first >80% of the cell cycle, but following an asymmetrical division, the small daughter grew at a faster exponential rate than the large daughter, an observation that potentially challenges present models of growth regulation. These growth and division behaviors place strong constraints on quantitative mechanistic descriptions of the cell cycle and growth control.


2007 ◽  
Vol 51 (4) ◽  
pp. 642-655 ◽  
Author(s):  
Nathalie Gonzalez ◽  
Frédéric Gévaudant ◽  
Michel Hernould ◽  
Christian Chevalier ◽  
Armand Mouras

2017 ◽  
Vol 92 (6) ◽  
pp. 1143-1156 ◽  
Author(s):  
Wenwei Xiong ◽  
Chunlei Wang ◽  
Xiangbo Zhang ◽  
Qinghua Yang ◽  
Ruixin Shao ◽  
...  

2017 ◽  
Vol 174 (2) ◽  
pp. 1127-1138 ◽  
Author(s):  
Yan-Zhuo Yang ◽  
Shuo Ding ◽  
Yong Wang ◽  
Cui-Ling Li ◽  
Yun Shen ◽  
...  

2021 ◽  
Author(s):  
Shixuan Liu ◽  
Ceryl Tan ◽  
Chloe Melo-Gavin ◽  
Kevin G. Mark ◽  
Miriam Bracha Ginzberg ◽  
...  

Proliferating animal cells maintain a stable size distribution over generations despite fluctuations in cell growth and division size. This tight control of cell size involves both cell size checkpoints (e.g., delaying cell cycle progression for small cells) and size-dependent compensation in rates of mass accumulation (e.g., slowdown of cellular growth in large cells). We previously identified that the mammalian cell size checkpoint is mediated by a selective activation of the p38 MAPK pathway in small cells. However, mechanisms underlying the size-dependent compensation of cellular growth remain unknown. In this study, we quantified global rates of protein synthesis and degradation in naturally large and small cells, as well as in conditions that trigger a size-dependent compensation in cellular growth. Rates of protein synthesis increase proportionally with cell size in both perturbed and unperturbed conditions, as well as across cell cycle stages. Additionally, large cells exhibit elevated rates of global protein degradation and increased levels of activated proteasomes. Conditions that trigger a large-size-induced slowdown of cellular growth also promote proteasome-mediated global protein degradation, which initiates only after growth rate compensation occurs. Interestingly, the elevated rates of global protein degradation in large cells were disproportionately higher than the increase in size, suggesting activation of protein degradation pathways. Large cells at the G1/S transition show hyperactivated levels of protein degradation, even higher than similarly sized or larger cells in S or G2, coinciding with the timing of the most stringent size control in animal cells. Together, these findings suggest that large cells maintain cell size homeostasis by activating global protein degradation to induce a compensatory slowdown of growth.


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