Non‐overlapping expression patterns of the clustered Dll‐A/B genes in the ascidian Ciona Intestinalis

Abstract

The Ci-Dll-A and Ci-Dll-B genes of Ciona intestinalis are arranged in a convergently transcribed gene cluster. This genomic arrangement is similar to that of the multiple bigene clusters of the Dlx homologs in vertebrates. Analysis of whole genome sequences showed that linkage to the Hox cluster is conserved with the vertebrate clusters. Phylogenetic analysis supports gene trees consistent with homology of the ascidian and vertebrate Dlx clusters, and in combination with the apparent conservation of genomic arrangement, it is concluded that the ascidian cluster is most likely homologous with the vertebrate clusters. Using whole-mount in situ hybridization, Ci-Dll-B transcripts were detected in all ectodermal lineages through gastrulation. Expression is radically downregulated in the neurula with detectable expression disappearing around the time that Ci-Dll-A expression appears in the anterior ectoderm. By the late tailbud stage Ci-Dll-Atranscripts were detected in the bilateral atrial primordia and persisted in the atrial rudiments to the larval stage, suggesting a role in development of these neural placode-like structures. This non-overlapping expression contradicts a common pattern seen in clustered genes, where as adjacent paralogs have largely overlapping expression domains. Enhancer sharing is often proposed as an explanation for the overlapping expression of gene cluster members. For this case of non-overlapping expression a model is proposed in which repressors acting at different stages override one or more shared enhancers. The enhancer sharing prevents breakup of the cluster while the independent temporal suppressors hide the presence of the shared enhancers.

Ephrin-mediated restriction of ERK1/2 activity delimits the number of pigment cells in the Ciona CNS

“…We inhibited MEK/ERK signal transduction by applying U0126, an inhibitor of the MAP kinase kinase, MEK1/2, at precise developmental time points. The following markers were used to assess neural plate patterning: FoxC (rows V and VI), Dll-B (epidermis and rows V and VI), ZicL (rows III and IV), Six3/6 (row IV), Mitf and Trp (row III) (Abitua et al, 2012; Irvine et al, 2007; Wagner and Levine, 2012). As reported previously, application of U0126 at the 76-cell stage disrupts the choice between row III/IV and row V/VI fates (Wagner and Levine, 2012).…”

Vertebrate Cranial Placodes as Evolutionary Innovations—The Ancestor's Tale

“…6). While the neural ectoderm in Ciona expresses Zic and SoxB1, the Dlx2/3/5 homologue DllB, AP2, and GATA1/2/3 (but not FoxI) are widely expressed in nonneural ectoderm (Christiaen et al, 2002;Imai, Hino, Yagi, Satoh, & Satou, 2004;Imai, Levine, Satoh, & Satou, 2006;Irvine, Cangiano, Millette, & Gutter, 2007;Mazet et al, 2005;Miya & Nishida, 2003;Wada, Katsuyama, & Saiga, 1999;Wada & Saiga, 2002). DllB expression also covers nonneural rows V and VI of the "neural plate" and is required for activating epidermal and palp markers (Imai et al, 2006;Irvine, Vierra, Millette, Blanchette, & Holbert, 2011).…”

“…It is still unclear how the oral siphon primordium (OSP), which has been fate-mapped to central row III/IV cells in Halocynthia (Nishida, 1987), escapes commitment to a neural fate. Upregulation of the Dlx1/4/6 homologue DllA as well as Pitx, and Six1/2 in this domain at early tailbud stages possibly plays a role here (Boorman & Shimeld, 2002;Caracciolo, DiGregorio, Aniello, Dilauro, & Branno, 2000;Christiaen et al, 2002;Irvine et al, 2007;Mazet et al, 2005).…”

Annelid Distal-less/Dlx duplications reveal varied post-duplication fates

“…The urochordate Ciona intestinalis possesses three Dlx genes, two of which are arranged in a tail-to-tail orientation. All three of the genes are closely linked to CiHox13 and CiHox12 (the Hox cluster is dispersed in C. intestinalis , and CiHox13 and CiHox12 exist as a bigene cluster; [20]). The divergent nature of the C. intestinalis Dlx sequences has made the deduction of clear gene orthologies difficult, but it is thought that the paired ascidian Dlx genes are a result of the same duplication that led to the paired arrangement of Dlx genes in the vertebrates [20].…”