scholarly journals Symmetry Breaking in Plants: Molecular Mechanisms Regulating Asymmetric Cell Divisions in Arabidopsis

2009 ◽  
Vol 1 (5) ◽  
pp. a000497-a000497 ◽  
Author(s):  
J. J. Petricka ◽  
J. M. Van Norman ◽  
P. N. Benfey
Keyword(s):  
Symmetry Breaking ◽  
Molecular Mechanisms ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions

scholarly journals Semaphorin signaling via MICAL3 induces symmetric cell division to expand breast cancer stem-like cells

2018 ◽  
Vol 116 (2) ◽  
pp. 625-630 ◽  
Author(s):  
Kana Tominaga ◽  
Hiroshi Minato ◽  
Takahiko Murayama ◽  
Asako Sasahara ◽  
Tatsunori Nishimura ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Mechanisms ◽  
Breast Cancer Patients ◽  
Asymmetric Cell Divisions ◽  
Symmetric Division ◽  
Cell Divisions ◽  
Tumor Sphere ◽  
Neuropilin 1 ◽  
Niche Factor ◽  
Sphere Formation

Cancer stem-like cells (CSCs) are expanded in the CSC niche by increased frequency of symmetric cell divisions at the expense of asymmetric cell divisions. The symmetric division of CSCs is important for the malignant properties of cancer; however, underlying molecular mechanisms remain largely elusive. Here, we show a cytokine, semaphorin 3 (Sema3), produced from the CSC niche, induces symmetric divisions of CSCs to expand the CSC population. Our findings indicate that stimulation with Sema3 induced sphere formation in breast cancer cells through neuropilin 1 (NP1) receptor that was specifically expressed in breast CSCs (BCSCs). Knockdown of MICAL3, a cytoplasmic Sema3 signal transducer, greatly decreased tumor sphere formation and tumor-initiating activity. Mechanistically, Sema3 induced interaction among MICAL3, collapsin response mediator protein 2 (CRMP2), and Numb. It appears that activity of MICAL3 monooxygenase (MO) stimulated by Sema3 is required for tumor sphere formation, interaction between CRMP2 and Numb, and accumulation of Numb protein. We found that knockdown of CRMP2 or Numb significantly decreased tumor sphere formation. Moreover, MICAL3 knockdown significantly decreased Sema3-induced symmetric divisions in NP1/Numb-positive BCSCs and increased asymmetric division that produces NP1/Numb negative cells without stem-like properties. In addition, breast cancer patients with NP1-positive cancer tissues show poor prognosis. Therefore, the niche factor Sema3-stimulated NP1/MICAL3/CRMP2/Numb axis appears to expand CSCs at least partly through increased frequency of MICAL3-mediated symmetric division of CSCs.

scholarly journals Spindle alignment is uncoupled with Kar9 symmetry breaking

2020 ◽  
Author(s):  
Miram Meziane ◽  
Rachel Genthial ◽  
Jackie Vogel
Keyword(s):  
Symmetry Breaking ◽  
Budding Yeast ◽  
Temporal Correlation ◽  
Spindle Positioning ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions

ABSTRACTSpindle positioning must be tightly regulated to ensure asymmetric cell divisions are successful. In budding yeast, spindle positioning is mediated by the asymmetric localization of microtubule +end tracking protein Kar9. Kar9 asymmetry is believed to be essential for spindle alignment. However, the temporal correlation between symmetry breaking and spindle alignment has not been measured. Here, we establish a method of quantifying Kar9 symmetry breaking and find that Kar9 asymmetry is not well coupled with early spindle alignment. We report the majority of asymmetric cells are not stably aligned. Rather, stable alignment, a state we define as perfect alignment, is correlated with Kar9 localization to the bud compartment, regardless of symmetry state. Our findings suggest that Kar9 asymmetry alone is insufficient for perfect alignment and reveal a possible role for Swe1 in regulating spindle alignment efficiency.

scholarly journals Kar9 symmetry breaking alone is insufficient to ensure spindle alignment

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Miram Meziane ◽  
Rachel Genthial ◽  
Jackie Vogel
Keyword(s):  
Symmetry Breaking ◽  
Budding Yeast ◽  
Temporal Correlation ◽  
Spindle Positioning ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions

AbstractSpindle positioning must be tightly regulated to ensure asymmetric cell divisions are successful. In budding yeast, spindle positioning is mediated by the asymmetric localization of microtubule + end tracking protein Kar9. Kar9 asymmetry is believed to be essential for spindle alignment. However, the temporal correlation between symmetry breaking and spindle alignment has not been measured. Here, we establish a method of quantifying Kar9 symmetry breaking and find that Kar9 asymmetry is not well coupled with stable spindle alignment. We report the spindles are not aligned in the majority of asymmetric cells. Rather, stable alignment is correlated with Kar9 residence in the bud, regardless of symmetry state. Our findings suggest that Kar9 asymmetry alone is insufficient for stable alignment and reveal a possible role for Swe1 in regulating Kar9 residence in the bud.

scholarly journals Tuning of self-renewing capacity in the Arabidopsis stomatal lineage by hormonal and nutrition regulation of asymmetric cell divisions

2020 ◽  
Author(s):  
Yan Gong ◽  
Julien Alassimone ◽  
Rachel Varnau ◽  
Nidhi Sharma ◽  
Lily S. Cheung ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Molecular Mechanisms ◽  
Leaf Size ◽  
Negative Regulator ◽  
Environmental Signals ◽  
Glucose Signaling ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions ◽  
Asymmetric Divisions ◽  
Stomatal Lineage

ABSTRACTAsymmetric and self-renewing divisions build and pattern tissues. In the Arabidopsis thaliana stomatal lineage, asymmetric cell divisions, guided by polarly localized cortical proteins, generate the majority of cells on the leaf surface. These divisions can be fine-tuned by systemic and environmental signals to modify tissue development, but the molecular mechanisms by which plants incorporate such cues to regulate asymmetric divisions are largely unknown. In a screen for modulators of cell polarity and asymmetric divisions, we identified a mutation in CONSTITIUTIVE TRIPLE RESPONSE 1, a negative regulator of ethylene signaling. We subsequently revealed antagonistic impacts of ethylene and glucose signaling on the self-renewing capacity of stomatal lineage stem cells. Quantitative analysis of the impacts of these signaling systems on cell polarity and fate dynamics showed that developmental information may be encoded in both the spatial and temporal asymmetries of polarity proteins. Taken together, our results provide a framework for a mechanistic understanding of how systemic information such as nutritional status and environmental factors tune stem cell behavior in the stomatal lineage, ultimately enabling optimization of leaf size and cell-type composition.

The Caenorhabditis elegans gene lin-44 controls the polarity of asymmetric cell divisions

Development ◽  
1994 ◽  
Vol 120 (5) ◽  
pp. 1035-1047 ◽  
Author(s):  
M.A. Herman ◽  
H.R. Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
The Body ◽  
Body Axis ◽  
Nematode Caenorhabditis Elegans ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions ◽  
Sister Cells

The generation and orientation of cellular and organismic polarity are fundamental aspects of development. Mutations in the gene lin-44 of the nematode Caenorhabditis elegans reverse both the relative positions of specific sister cells and the apparent polarities of these cells. Thus, lin-44 mutants appear to generate polar cells but to misorient these cells along the body axis of the animal. We postulate that lin-44 acts to specify the orientation of polar cells.

discordia mutations specifically misorient asymmetric cell divisions during development of the maize leaf epidermis

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4623-4633 ◽  
Author(s):  
K. Gallagher ◽  
L.G. Smith
Keyword(s):  
Cell Division ◽  
Preprophase Band ◽  
Cytochalasin D ◽  
Leaf Epidermis ◽  
Asymmetric Cell Divisions ◽  
Maize Leaf ◽  
Cell Divisions ◽  
Cytoskeletal Structure ◽  
Dividing Cells ◽  
Preprophase Bands

In plant cells, cytokinesis depends on a cytoskeletal structure called a phragmoplast, which directs the formation of a new cell wall between daughter nuclei after mitosis. The orientation of cell division depends on guidance of the phragmoplast during cytokinesis to a cortical site marked throughout prophase by another cytoskeletal structure called a preprophase band. Asymmetrically dividing cells become polarized and form asymmetric preprophase bands prior to mitosis; phragmoplasts are subsequently guided to these asymmetric cortical sites to form daughter cells of different shapes and/or sizes. Here we describe two new recessive mutations, discordia1 (dcd1) and discordia2 (dcd2), which disrupt the spatial regulation of cytokinesis during asymmetric cell divisions. Both mutations disrupt four classes of asymmetric cell divisions during the development of the maize leaf epidermis, without affecting the symmetric divisions through which most epidermal cells arise. The effects of dcd mutations on asymmetric cell division can be mimicked by cytochalasin D treatment, and divisions affected by dcd1 are hypersensitive to the effects of cytochalasin D. Analysis of actin and microtubule organization in these mutants showed no effect of either mutation on cell polarity, or on formation and localization of preprophase bands and spindles. In mutant cells, phragmoplasts in asymmetrically dividing cells are structurally normal and are initiated in the correct location, but often fail to move to the position formerly occupied by the preprophase band. We propose that dcd mutations disrupt an actin-dependent process necessary for the guidance of phragmoplasts during cytokinesis in asymmetrically dividing cells.

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