scholarly journals Epidermal Patterning Genes Impose Non-cell Autonomous Cell Size Determination and have Additional Roles in Root Meristem Size Control

2013 ◽  
Vol 55 (9) ◽  
pp. 864-875 ◽  
Author(s):  
Christian Löfke ◽  
Kai Dünser ◽  
Jürgen Kleine-Vehn
2021 ◽  
Author(s):  
Toshisagba Longkumer ◽  
Chih-Yun Chen ◽  
Marco Biancucci ◽  
Bhaskara Govinal Badiger ◽  
Paul E. Verslues

During moderate severity drought and low water potential (Ψw) stress, poorly understood signaling mechanisms restrict both meristem cell division and subsequent cell expansion. We found that the Clade E Growth-Regulating 2 (EGR2) protein phosphatase and Microtubule Associated Stress Protein 1 (MASP1) differed in their stoichiometry of expression across the root meristem and had opposing effects on root meristem activity at low Ψw. Ectopic MASP1 or EGR expression increased or decreased, respectively, root meristem size and root elongation during low Ψw stress. This, along with the ability of phosphomimic MASP1 to overcome EGR suppression of root meristem size and observation that ectopic EGR expression had no effect on unstressed plants, indicated that during low Ψw EGR activation and attenuation of MASP1 phosphorylation in their overlapping zone of expression determines root meristem size and activity. Ectopic EGR expression also decreased root cell size at low Ψw. Conversely, both the egr1-1egr2-1 and egr1-1egr2-1masp1-1 mutants had similarly increased root cell size; but, only egr1-1egr2-1 had increased cell division. These observations demonstrated that EGRs affect meristem activity via MASP1 but affect cell expansion via other mechanisms. Interestingly, EGR2 was highly expressed in the root cortex, a cell type important for growth regulation and environmental response.


2021 ◽  
Vol 22 (9) ◽  
pp. 4731
Author(s):  
Jacob P. Rutten ◽  
Kirsten H. Ten Tusscher

After germination, the meristem of the embryonic plant root becomes activated, expands in size and subsequently stabilizes to support post-embryonic root growth. The plant hormones auxin and cytokinin, together with master transcription factors of the PLETHORA (PLT) family have been shown to form a regulatory network that governs the patterning of this root meristem. Still, which functional constraints contributed to shaping the dynamics and architecture of this network, has largely remained unanswered. Using a combination of modeling approaches we reveal how the interplay between auxin and PLTs enables meristem activation in response to above-threshold stimulation, while its embedding in a PIN-mediated auxin reflux loop ensures localized PLT transcription and thereby, a finite meristem size. We furthermore demonstrate how this constrained PLT transcriptional domain enables independent control of meristem size and division rates, further supporting a division of labor between auxin and PLT. We subsequently reveal how the weaker auxin antagonism of the earlier active Arabidopsis response regulator 12 (ARR12) may arise from the absence of a DELLA protein interaction domain. Our model indicates that this reduced strength is essential to prevent collapse in the early stages of meristem expansion while at later stages the enhanced strength of Arabidopsis response regulator 1 (ARR1) is required for sufficient meristem size control. Summarizing, our work indicates that functional constraints significantly contribute to shaping the auxin–cytokinin–PLT regulatory network.


2013 ◽  
Vol 8 (6) ◽  
pp. e24226 ◽  
Author(s):  
Yuancheng Peng ◽  
Liangliang Chen ◽  
Yaru Lu ◽  
Wenying Ma ◽  
Yiping Tong ◽  
...  

2007 ◽  
Vol 306 (1) ◽  
pp. 339 ◽  
Author(s):  
Andres Dekanty ◽  
Lazaro Centanin ◽  
Pablo Wappner

2000 ◽  
Vol 3 (6) ◽  
pp. 488-492 ◽  
Author(s):  
Eva Kondorosi ◽  
François Roudier ◽  
Emmanuel Gendreau

2016 ◽  
Author(s):  
Morgan Delarue ◽  
Daniel Weissman ◽  
Oskar Hallatschek

AbstractIncreasingly accurate and massive data have recently shed light on the fundamental question of how cells maintain a stable size trajectory as they progress through the cell cycle. Microbes seem to use strategies ranging from a pure sizer, where the end of a given phase is triggered when the cell reaches a critical size, to pure adder, where the cell adds a constant size during a phase. Yet the biological origins of the observed spectrum of behavior remain elusive. We analyze a molecular size-control mechanism, based on experimental data from the yeast S. cerevisiae, that gives rise to behaviors smoothly interpolating between adder and sizer. The size-control is obtained from the titration of a repressor protein by an activator protein that accumulates more rapidly with increasing cell size. Strikingly, the size-control is composed of two different regimes: for small initial cell size, the size-control is a sizer, whereas for larger initial cell size, is is an imperfect adder. Our model thus indicates that the adder and critical size behaviors may just be different dynamical regimes of a single simple biophysical mechanism.


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