Effects of the Brachyury (T) mutation on morphogenetic movement in the mouse embryo

Yanagisawa, Keiji; Fujimoto, Hirokazu; Urushihara, Hideko

doi:10.1016/0012-1606(81)90147-0

Cited by 99 publications

(45 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At this time, cell death is visible in ntl and in compound mutants, and probably leads to the subsequent truncation and/or loss of posterior tissues. In support of this, Xenopus embryos with perturbed brachyury function and brachyury mouse mutants only exhibit apoptosis in posterior tissues after gastrulation defects are apparent (Chesley, 1935;Conlon and Smith, 1999;Yanagisawa et al, 1981). This increase in programmed cell death was proposed to be an indirect consequence of altered adhesion as reported for epithelial cells that occupy an inappropriate location (Conlon and Smith, 1999;Khwaja et al, 1997).…”

Section: Aberrant Cell Proliferation and Death Do Not Account For Earmentioning

confidence: 81%

No tail co-operates with non-canonical Wnt signaling to regulate posterior body morphogenesis in zebrafish

et al. 2004

View full text Add to dashboard Cite

The vertebrate posterior body is formed by a combination of the gastrulation movements that shape the head and anterior trunk and posterior specific cell behaviors. Here, we investigated whether genes that regulate cell movements during gastrulation [no tail(ntl)/brachyury, knypek (kny) and pipetail(ppt)/wnt5] interact to regulate posterior body morphogenesis. Both kny;ntl and ppt;ntl double mutant embryos exhibit synergistic trunk and tail shortening by early segmentation. Gene expression analysis in the compound mutants indicates that anteroposterior germ-layer patterning is largely normal and that the tail elongation defects are not due to failure to specify or maintain posterior tissues. Moreover, ntl interacts with ppt and knyto synergistically regulate the posterior expression of the gene encoding bone morphogenetic protein 4 (bmp4) but not of other known T-box genes,fibroblast growth factor genes or caudal genes. Examination of mitotic and apoptotic cells indicates that impaired tail elongation is not simply due to decreased cell proliferation or increased cell death. Cell tracing in ppt;ntl and kny;ntl mutants demonstrates that the ventral derived posterior tailbud progenitors move into the tailbud. However,gastrulation-like convergence and extension movements and cell movements within the posterior tailbud are impaired. Furthermore, subduction movements of cells into the mesendoderm are reduced in kny;ntl and ppt;ntl mutants. We propose that Ntl and the non-canonical Wnt pathway components Ppt and Kny function in parallel, partially redundant pathways to regulate posterior body development. Our work initiates the genetic dissection of posterior body morphogenesis and links genes to specific tail-forming movements. Moreover, we provide genetic evidence for the notion that tail development entails a continuation of mechanisms regulating gastrulation together with mechanisms unique to the posterior body.

show abstract

Section: Aberrant Cell Proliferation and Death Do Not Account For Earmentioning

confidence: 81%

No tail co-operates with non-canonical Wnt signaling to regulate posterior body morphogenesis in zebrafish

et al. 2004

View full text Add to dashboard Cite

show abstract

“…By embryonic day eight (E8), the mesoderm: ectoderm ratio is elevated 15% in the posterior portions of mutant embryos while remaining normal in the anterior half (Yanagisawa et al, 1981). Because the mitotic index of both the anterior and posterior portions of T -/-embryos appears normal, the primary defect appears to be an alteration in cell adhesion (Yanagisawa and Fujimoto, 1977;Yanagisawa et al, 1981). In support of such a hypothesis, measurements of mesodermal migration on an extracellular matrix show a reduction in the migration of mutant-derived mesodermal cells relative to wild-type (Hashimoto et al, 1987).…”

Section: Brachyury and Early Development In The Mousementioning

confidence: 99%

T‐box genes in early embryogenesis

Showell

Binder

Conlon

2003

Developmental Dynamics

271

229

View full text Add to dashboard Cite

“…Brachyury -/-gastrulae generate insufficient mesoderm, and posterior structures are absent at later embryonic stages (Chesley, 1935;Yanagisawa et al, 1981;Herrmann et al, 1990;Wilkinson et al, 1990). Other T-box genes such as Drosophila optomotor-blind and mouse Tbx6 also specify tissue fate and control posteriorization during development (Kopp and Duncan, 1997;Chapman and Papaioannou, 1998).…”

Section: Introductionmentioning

confidence: 99%

Suppression of neural fate and control of inner ear morphogenesis byTbx1

et al. 2004

View full text Add to dashboard Cite

Inner ear sensory organs and VIIIth cranial ganglion neurons of the auditory/vestibular pathway derive from an ectodermal placode that invaginates to form an otocyst. We show that in the mouse otocyst epithelium, Tbx1 suppresses neurogenin 1-mediated neural fate determination and is required for induction or proper patterning of gene expression related to sensory organ morphogenesis (Otx1 and Bmp4, respectively). Tbx1 loss-of-function causes dysregulation of neural competence in otocyst regions linked to the formation of either mechanosensory or structural sensory organ epithelia. Subsequently, VIIIth ganglion rudiment form is duplicated posteriorly, while the inner ear is hypoplastic and shows neither a vestibular apparatus nor a coiled cochlear duct. We propose that Tbx1acts in the manner of a selector gene to control neural and sensory organ fate specification in the otocyst.

show abstract

Effects of the Brachyury (T) mutation on morphogenetic movement in the mouse embryo

Cited by 99 publications

References 7 publications

No tail co-operates with non-canonical Wnt signaling to regulate posterior body morphogenesis in zebrafish

No tail co-operates with non-canonical Wnt signaling to regulate posterior body morphogenesis in zebrafish

T‐box genes in early embryogenesis

Suppression of neural fate and control of inner ear morphogenesis byTbx1

Contact Info

Product

Resources

About