HMG and Helper sites contribute differentially to the regulation of <i>end-1</i> during early embryogenesis.

Abstract

<p>Deconvolved (A–C) and Nomarski (A′–C′) images showing expression of a stably integrated <i>end-1::GFP::H2B</i> reporter in the endodermal (E) and/or mesodermal (MS) daughters of live embryos at the 2E stage. The wild type (WT) reporter shows strong GFP expression in the E cell daughters (A, A′). Mutation of the HMG site leads to a significant reduction of GFP expression in the E daughters and a significant derepression of <i>end-1::GFP::H2B</i> in the MS daughters (B, B′). Mutation of two Helper sites leads to a significant reduction of GFP in the E daughters (C, C′), but little or no depression in the MS daughters (C, C′). (D) Histograms summarizing the results from over 100 embryos from three independent lines for each construct, grouped by strong, weak or no expression in the E (upper graph) and MS (lower graph) cells.</p