dictyNews
Electronic Edition
Volume 45, number 12
April 19, 2019
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Abstracts
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The fate of cells undergoing spontaneous DNA damage during
development
Agnes Miermont, Vlatka Antolovic, Tchern Lenn, John M. E. Nichols,
Lindsey J. Millward, Jonathan R. Chubb
Development, in press
Embryonic development involves extensive and often rapid cell
proliferation. An unavoidable side effect of cell proliferation is DNA
damage. The consequences of spontaneous DNA damage during
development are not clear. Here we define an approach to determine
the effects of DNA damage on cell fate choice. Using single cell
transcriptomics, we identified a sub-population of Dictyostelium cells
experiencing spontaneous DNA damage. Damaged cells displayed
high expression of rad51, with the gene induced by multiple types of
genotoxic stress. Using live imaging, we tracked high Rad51 cells
from differentiation onset until cell fate assignment. High Rad51 cells
were shed from multicellular structures, excluding damaged cells
from the spore population. Cell shedding resulted from impaired cell
motility and defective cell-cell adhesion, with damaged cells
additionally defective in activation of spore gene expression. These
data indicate DNA damage is not insulated from other aspects of cell
physiology during development and multiple features of damaged
cells prevent propagation of genetic error. Our approach is generally
applicable for monitoring rare sub-populations during development,
and permits analysis of developmental perturbations occurring within
a physiological dynamic range.
submitted by: Jonathan Chubb [[log in to unmask]]
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Derivatives of Dictyostelium differentiation-inducing factors inhibit
serum-dependent cell migration of murine osteosarcoma LM8 cells
Yuzuru Kubohara 1,2,*, Haruhisa Kikuchi 3, Yoshiteru Oshima 3,4
1 Laboratory of Health and Life Science, Juntendo University Graduate
School of Health and Sports Science, Inzai, Chiba 270-1695, Japan
2 Department of Molecular and Cellular Biology, Institute for Molecular
and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512,
Japan
3 Laboratory of Natural Products Chemistry, Tohoku University Graduate
School of Pharmaceutical Sciences, Aoba-ku, Sendai 980-8578, Japan
4 United Centers for Advanced Research and Translational Medicine
(ART), Tohoku University Graduate School of Medicine, Aoba-ku,
Sendai 980-8575, Japan
*Corresponding author
Juntendo Medical Journal (Open access J.)
(https://www.jstage.jst.go.jp/article/jmj/65/1/65_JMJ18-OA10/_pdf/-char/en)
Objective: Differentiation-inducing factor-1 (DIF-1) and -3 are novel lead
anti-tumor agents that were originally isolated from the cellular slime mold
Dictyostelium discoideum. We previously showed that the DIF derivatives
Br-DIF-1, DIF-3(+2), and Bu-DIF-3 strongly suppress lysophosphatidic acid
(LPA)-induced cell migration in mouse osteosarcoma LM8 cells in vitro.
Here, we investigated the effects of these three DIF derivatives on the cell
migration (wound healing) of LM8 cells and mouse 3T3-L1 fibroblast cells
(a model of non-transformed cells).
Methods: A wound healing assay was performed to estimate the anti-cell
migration activities of the compounds; cell growth was assessed by using
a cell number indicator.
Results: After monolayers of LM8 cells or 3T3-L1 cells were wounded by
scratching and incubated with 10% serum-containing media for 20 h or 8 h,
respectively, cell-free areas (wounds) in the monolayer were occupied
(healed) by neighboring cells to some extent even in the presence of Ara-C
(an inhibitor of cell proliferation). This phenomenon is attributed to the
migration of the neighboring cells into the wounds. Wound healing (cell
migration) of LM8 cells was strongly suppressed in the presence of 10 uM
Br-DIF-1, DIF-3(+2), or Bu-DIF-3. These DIF derivatives more effectively
suppressed the cell migration of LM8 cells than of 3T3-L1 cells.
Conclusion: The results support our expectation that these DIF derivatives
are promising lead anti-metastatic agents that may not affect normal cell
migration.
submitted by: Yuzuru Kubohara [[log in to unmask]]
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