Dorsoventral Patterning in Hemichordates: Insights into Early Chordate Evolution

We report here the genetical and molecular characterization of a new Drosophila zygotic lethal locus, vrille (vri). vri alleles act not only as dominant maternal enhancers of embryonic dorsoventral patterning defects caused by easter and decapentaplegic (dpp) mutations, but also as dominant zygotic enhancers of dpp alleles for phenotypes in wing. The vri gene encodes a new member of the bZIP family of transcription factors closely related to gene 9 of Xenopus laevis, induced by thyroid hormone during the tadpole tail resorption program, and NF-IL3A, a human T cell transcription factor that transactivates the interleukin-3 promoter. NF-IL3A shares 93% similarity and 60% identity with Vri for a stretch of 68 amino acids that includes the bZIP domain. Although all the alleles tested behave like antimorphs, the dominant enhancement is also seen with a nonsense mutation allele that prevents translation of the bZIP domain. Because of the strong dominant enhancement of dpp phenotypes by vri alleles in both embryo and wing, and also the similarity between the wing vein phenotypes caused by the vri and shortvein dpp alleles, we postulate that vri interacts either directly or indirectly with certain components of the dpp (a TGFβ homologue) signal transduction pathway.

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Conserved and unique transcriptional features of pharyngeal arches in the skate (Leucoraja erinacea) and evolution of the jaw

Molecular Biology and Evolution ◽

10.1093/molbev/msab123 ◽

2021 ◽

Author(s):

Christine Hirschberger ◽

Victoria A Sleight ◽

Katharine E Criswell ◽

Stephen J Clark ◽

J Andrew Gillis

Keyword(s):

Evolutionary Biology ◽

Gill Arch ◽

Dorsoventral Patterning ◽

Pharyngeal Arches ◽

Mandibular Arch ◽

Serial Homology ◽

Expression Of Genes ◽

Developmental Patterning ◽

Genes Encoding ◽

Differential Gene

Abstract The origin of the jaw is a long-standing problem in vertebrate evolutionary biology. Classical hypotheses of serial homology propose that the upper and lower jaw evolved through modifications of dorsal and ventral gill arch skeletal elements, respectively. If the jaw and gill arches are derived members of a primitive branchial series, we predict that they would share common developmental patterning mechanisms. Using candidate and RNAseq/differential gene expression analyses, we find broad conservation of dorsoventral patterning mechanisms within the developing mandibular, hyoid and gill arches of a cartilaginous fish, the skate (Leucoraja erinacea). Shared features include expression of genes encoding members of the ventralising BMP and endothelin signalling pathways and their effectors, the joint markers nkx3.2 and gdf5 and pro-chondrogenic transcription factor barx1, and the dorsal territory marker pou3f3. Additionally, we find that mesenchymal expression of eya1/six1 is an ancestral feature of the mandibular arch of jawed vertebrates, while differences in notch signalling distinguish the mandibular and gill arches in skate. Comparative transcriptomic analyses of mandibular and gill arch tissues reveal additional genes differentially expressed along the dorsoventral axis of the pharyngeal arches, including scamp5 as a novel marker of the dorsal mandibular arch, as well as distinct transcriptional features of mandibular and gill arch muscle progenitors and developing gill buds. Taken together, our findings reveal conserved patterning mechanisms in the pharyngeal arches of jawed vertebrates, consistent with serial homology of their skeletal derivatives, as well as unique transcriptional features that may underpin distinct jaw and gill arch morphologies.

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A group of genes required for maintenance of the amnioserosa tissue in Drosophila

Development ◽

10.1242/dev.122.5.1343 ◽

1996 ◽

Vol 122 (5) ◽

pp. 1343-1352 ◽

Cited By ~ 5

Author(s):

L.H. Frank ◽

C. Rushlow

Keyword(s):

Cell Death ◽

Cell Loss ◽

Dorsal Side ◽

Drosophila Embryo ◽

Epithelial Tissue ◽

Dorsoventral Patterning ◽

Wild Type ◽

Germ Band ◽

Initial Development

The amnioserosa is an extraembryonic, epithelial tissue that covers the dorsal side of the Drosophila embryo. The initial development of the amnioserosa is controlled by the dorsoventral patterning genes. Here we show that a group of genes, which we refer to as the U-shaped-group (ush-group), is required for maintenance of the amnioserosa tissue once it has differentiated. Using several molecular markers, we examined amnioserosa development in the ush-group mutants: u-shaped (ush), hindsight (hnt), serpent (srp) and tail-up (tup). Our results show that the amnioserosa in these mutants is specified correctly and begins to differentiate as in wild type. However, following germ-band extension, there is a premature loss of the amnioserosa. We demonstrate that this cell loss is a consequence of programmed cell death (apoptosis) in ush, hnt and srp, but not in tup. We discuss the role of the ush-group genes in maintaining the amnioserosa's viability. We also discuss a possible role for the amnioserosa in germ-band retraction in light of these mutants' unretracted phenotype.

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Proteolytic cleavage of Chordin as a switch for the dual activities of Twisted gastrulation in BMP signaling

Development ◽

10.1242/dev.128.22.4439 ◽

2001 ◽

Vol 128 (22) ◽

pp. 4439-4447 ◽

Cited By ~ 1

Author(s):

Juan Larraín ◽

Michael Oelgeschläger ◽

Nan I. Ketpura ◽

Bruno Reversade ◽

Lise Zakin ◽

...

Keyword(s):

Ternary Complex ◽

Binding Assay ◽

Bmp Signaling ◽

Dominant Negative ◽

Secreted Proteins ◽

Dorsoventral Patterning ◽

Twisted Gastrulation ◽

Cognate Receptor ◽

Licl Treatment ◽

Bmp Antagonist

Dorsoventral patterning is regulated by a system of interacting secreted proteins involving BMP, Chordin, Xolloid and Twisted gastrulation (Tsg). We have analyzed the molecular mechanism by which Tsg regulates BMP signaling. Overexpression of Tsg mRNA in Xenopus embryos has ventralizing effects similar to Xolloid, a metalloprotease that cleaves Chordin. In embryos dorsalized by LiCl treatment, microinjection of Xolloid or Tsg mRNA restores the formation of trunk-tail structures, indicating an increase in BMP signaling. Microinjection of Tsg mRNA leads to the degradation of endogenous Chordin fragments generated by Xolloid. The ventralizing activities of Tsg require an endogenous Xolloid-like activity, as they can be blocked by a dominant-negative Xolloid mutant. A BMP-receptor binding assay revealed that Tsg has two distinct and sequential activities on BMP signaling. First, Tsg makes Chordin a better BMP antagonist by forming a ternary complex that prevents binding of BMP to its cognate receptor. Second, after cleavage of Chordin by Xolloid, Tsg competes the residual anti-BMP activity of Chordin fragments and facilitates their degradation. This molecular pathway, in which Xolloid switches the activity of Tsg from a BMP antagonist to a pro-BMP signal once all endogenous full-length Chordin is degraded, may help explain how sharp borders between embryonic territories are generated.

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