Genetics - Research Publications

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    In vivo imaging and tracking of individual nanodiamonds in drosophila melanogaster embryos
    Simpson, DA ; Thompson, AJ ; Kowarsky, M ; Zeeshan, NF ; Barson, MSJ ; Hall, LT ; Yan, Y ; Kaufmann, S ; Johnson, BC ; Ohshima, T ; Caruso, F ; Scholten, RE ; Saint, RB ; Murray, MJ ; Hollenberg, LCL (OPTICAL SOC AMER, 2014-04-01)
    In this work, we incorporate and image individual fluorescent nanodiamonds in the powerful genetic model system Drosophila melanogaster. Fluorescence correlation spectroscopy and wide-field imaging techniques are applied to individual fluorescent nanodiamonds in blastoderm cells during stage 5 of development, up to a depth of 40 µm. The majority of nanodiamonds in the blastoderm cells during cellularization exhibit free diffusion with an average diffusion coefficient of (6 ± 3) × 10(-3) µm(2)/s, (mean ± SD). Driven motion in the blastoderm cells was also observed with an average velocity of 0.13 ± 0.10 µm/s (mean ± SD) µm/s and an average applied force of 0.07 ± 0.05 pN (mean ± SD). Nanodiamonds in the periplasm between the nuclei and yolk were also found to undergo free diffusion with a significantly larger diffusion coefficient of (63 ± 35) × 10(-3) µm(2)/s (mean ± SD). Driven motion in this region exhibited similar average velocities and applied forces compared to the blastoderm cells indicating the transport dynamics in the two cytoplasmic regions are analogous.
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    JNK signaling is needed to tolerate chromosomal instability
    Wong, HW-S ; Shaukat, Z ; Wang, J ; Saint, R ; Gregory, SL (LANDES BIOSCIENCE, 2014-02-15)
    Chromosomal instability (CIN), as a common feature of tumors, represents a potential therapeutic target if ways can be found to specifically cause apoptosis in unstably dividing cells. We have previously shown that if signaling through the JNK pathway is reduced, apoptosis is triggered in models of chromosomal instability induced by loss of the spindle checkpoint. Here we identify components upstream and downstream of JNK that are able to mediate this effect, and test the involvement of p53 and DNA damage in causing apoptosis when JNK signaling is reduced in CIN cells. We show that cell cycle progression timing has a strong effect on the apoptosis seen when JNK signaling is reduced in genetically unstable cells: a shortened G 2 phase enhances the apoptosis, while lengthening G 2 rescues the JNK-deficient CIN cell death phenotype. Our findings suggest that chromosomal instability represents a significant stress to dividing cells, and that without JNK signaling, cells undergo apoptosis because they lack a timely and effective response to DNA damage.