Dorso-ventral and rostro-caudal sequential expression of M-twist in the postimplantation murine embryo

Abstract

M-twist is the murine homolog of the Drosophila twist gene which is a zygotic target for maternal genes that establish embryonic dorso-ventral polarity and is necessary for mesoderm formation. We recently showed that before gastrulation, M-twist transcripts are detected in morulae and blastocysts, then in extra-embryonic tissues of early implanted mouse embryos before the onset of gastrulation, and we suggested that M-twist might be involved in embryonic polarity (Stoetzel et al., submitted). Here, using in situ hybridization on whole mount embryos, we present the expression pattern of M-twist from primitive streak stage up to 10.5 days p.c. In implanted embryos, M-twist is first expressed in extra-embryonic tissues, then in embryo proper around egg cylinder stage within some embryonic ectodermal cells of the primitive streak. Slightly later, scattered cells within the amniotic cavity apparently detached from the primitive streak also express the gene. Then, M-twist transcripts accumulate in head mesenchyme, the first aortic arches, somites and lateral mesoderm and, as development proceeds, successively the second, third and fourth branchial arches, the anterior limb buds and, finally, the posterior limb buds. Thus M-twist expression in implanted embryos occurs first along a dorso-ventral gradient pattern until the headfold stage, then it is gradually observed along the rostro-caudal axis of the embryos as development procedes in the mesodermal cell layer and in neural crest cell derivatives. In addition, we show the existence of some previously undescribed subsets of scattered cells that express M-twist and thus might participate in murine embryo development.

Mutations within or upstream of the basic helix–loop–helix domain of the TWIST gene are specific to Saethre-Chotzen syndrome

“…9,10 In vertebrates, this factor is apparently involved in negative control of cellular determination and in differentiation of several cell lineages including myogenesis, neurogenesis and osteogenesis. [11][12][13][14] The putative interactions between TWIST and Fibroblast Growth Factor Receptors (FGFRs) via a common signalling pathway are supported by the recent observation that several familial cases of ACS III-like craniosynostosis syndromes and sporadic cases originally diagnosed as ACS III, harboured the recurrent P250R FGFR 3 mutation in the extracellular region of the receptor. [15][16][17][18] Here we report on 16 additional TWIST mutations (including 11 novel mutations) in typical ACS III patients.…”

Msx2andTwistcooperatively control the development of the neural crest-derived skeletogenic mesenchyme of the murine skull vault

“…Msx2 and Twist are also co-expressed in developing limb (Coelho et al, 1991;Davidson et al, 1991;Robert et al, 1991;Fuchtbauer, 1995;Stoetzel et al, 1995), prompting us to ask whether the Msx2 genotype affected the penetrance of the anterior digit duplication characteristic of Twist +/-mice (Bourgeois et al, 1998). The incidence of the digit duplication phenotype in Twist +/-mice (34%, n=58) was identical to that in Msx2 +/-; Fig.…”

Expression of M‐twist during postimplantation development of the mouse

“…After this paper was submitted, Stoetzel et al (1995) published a study in which they show a similar espression pattern of M-twist between day 8 and 10 p.c. However, the data on M-twist expression in the primitive streak stage embryo do not match the ones presented here.…”