Reduced O2 and elevated ROS in sea urchin embryos leads to defects in ectoderm differentiation

Authors

  • Cavit Agca,

    1. Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, New Orleans, Louisiana
    2. Department of Biochemistry and Molecular Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
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  • William H. Klein,

    1. Department of Biochemistry and Molecular Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
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  • Judith M. Venuti

    Corresponding author
    1. Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, New Orleans, Louisiana
    • Department of Cell Biology and Anatomy, LSU Health Sciences Center, 1901 Perdido Street, New Orleans, LA
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Abstract

The sea urchin oral-aboral (OA) axis is established in part by Nodal signaling. The OA axis is also influenced by treatments affecting respiration and Nodal transcription is influenced by redox-dependent transcription factors. This suggests that intracellular redox state plays a role in OA axis specification. Since cellular redox state can be altered by the formation of excess reactive oxygen species (ROS), and hypoxia and paraquat generate ROS in cells, we asked whether these treatments affected specification of the OA axis and Nodal expression. Embryos cultured under conditions that elevate ROS, demonstrate perturbed ectoderm specification, but other territories are not affected. Immunohistochemical and Q-RT-PCR analyses revealed that both oral and aboral ectoderm genes are downregulated. Our results argue that elevating ROS in sea urchin embryos by these treatments blocks early steps in ectoderm differentiation preceding the polarization of the ectoderm into oral and aboral territories. Developmental Dynamics 238:1777–1787, 2009. © 2009 Wiley-Liss, Inc.

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