T-box gene<i>eomesodermin</i>and the homeobox-containing Mix/Bix gene<i>mtx2</i>regulate epiboly movements in the zebrafish

Bruce, Ashley E.E.; Howley, Cristin; Fox, Monica Dixon; Ho, Ruoya

doi:10.1002/dvdy.20305

Cited by 47 publications

(49 citation statements)

References 62 publications

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“…mtx2, which is expressed in the YSL and marginal cells (Hirata et al, 2000), appears to be regulated by the maternal factor Eomesodermin (Bruce et al, 2005). However, Eomesodermin does not appear to regulate mtx1 gene expression (Bruce et al, 2005), indicating that another maternal factor is involved. Interestingly, the phenotype of mtx1 MO-injected heterozygous natter embryos appears similar to that of the maternal mutant pollywog (Fig.…”

Section: Roles Of the Extra-embryonic Ysl In Myocardial Migrationmentioning

confidence: 93%

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The yolk syncytial layer regulates myocardial migration by influencing extracellular matrix assembly in zebrafish

et al. 2006

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The roles of extra-embryonic tissues in early vertebrate body patterning have been extensively studied, yet we know little about their function during later developmental events. Here, we analyze the function of the zebrafish extra-embryonic yolk syncytial layer (YSL) specific transcription factor, Mtx1, and find that it plays an essential role in myocardial migration. Downregulating the function of Mtx1 in the YSL leads to cardia bifida, a phenotype in which the myocardial cells fail to migrate to the midline. Mtx1 in the extra-embryonic YSL appears to regulate the embryonic expression of fibronectin, a gene previously implicated in myocardial migration. We further show dosage-sensitive genetic interactions between mtx1 and fibronectin. Based on these data, we propose that the extra-embryonic YSL regulates myocardial migration, at least in part by influencing fibronectin expression and subsequent assembly of the extracellular matrix in embryonic tissues.

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Section: Roles Of the Extra-embryonic Ysl In Myocardial Migrationmentioning

confidence: 93%

“…The yolk syncytial layer regulates myocardial migration by influencing extracellular matrix assembly in zebrafish (Kikuchi et al, 2000), and mtx2 appears to regulate epiboly movements (Bruce et al, 2005). However, the function of mtx1 remains unexplored.…”

Section: Introductionmentioning

confidence: 99%

The yolk syncytial layer regulates myocardial migration by influencing extracellular matrix assembly in zebrafish

et al. 2006

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“…(2) Embryos affected in Bmp signaling can differentiate into endoderm, and endoderm mutants do not fail in DV patterning. (3) DV patterning mutants, including strongly dorsalized Mspg embryos, undergo normal epiboly, and epiboly-defective embryos have normal DV and endoderm differentiation Bruce et al, 2005). (4) Mutants affected in endoderm formation, including strongly dorsalized Mspg embryos, have no arrest in epiboly, and vice versa.…”

Section: Three Independent Maternal Functions Of Pou2mentioning

confidence: 99%

Maternal control of vertebrate dorsoventral axis formation and epiboly by the POU domain protein Spg/Pou2/Oct4

2006

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Dorsoventral (DV) axis formation of the vertebrate embryo is controlled by the maternal genome and is subsequently refined zygotically. In the zygote, repression of ventralizing Bmp activity on the dorsal side through chordin and noggin is crucial for establishment of a dorsally located organizer. This interplay generates a zygotic Bmp activity gradient that defines distinct positional values along the DV axis. The maternal processes that control expression of the zygotic genes implicated in DV patterning are largely unknown. spiel-ohne-grenzen (spg/pou2) is a maternally and zygotically expressed zebrafish gene that encodes the POU domain transcription factor Pou2, an ortholog of mammalian Oct4/Pou5f1. We show that embryos that are genetically depleted of both maternal and zygotic pou2 function (MZspg) exhibit extreme DV patterning defects and, independently, a blastoderm-specific arrest of epiboly. Dorsal tissues expand to the ventral side at the expense of ventrolateral tissue in MZspg embryos. Dorsally expressed Bmp-antagonists, such as Chd and Nog1, and Gsc are ectopically activated at ventral levels in MZspg. Lack of ventral specification is apparent very early, suggesting that maternal processes are affected in MZspg. Indeed, maternal pou2 function is necessary to initiate zygotic expression of ventrally expressed genes such as bmp2b and bmp4, and for proper activation of bmp7, vox, vent and eve1. A constitutively active Alk8-TGF␤-receptor can ectopically induce bmp2b and bmp4 and rescues the dorsalization of MZspg. This indicates that pou2 acts upstream of Alk8, a maternally provided receptor implicated in the activation of zygotic bmp2b and bmp4 transcription. Consistent with this possibility, Bmp gene misexpression can rescue MZspg embryos, indicating that TGF␤-mediated signal transduction itself is intact in absence of Pou2. Inhibition of Fgf signaling, another pathway with early dorsalizing activity, can also restore and even ventralize MZspg embryos. The requirement for pou2 to initiate bmp2b expression can therefore be bypassed by releasing the repressive function of Fgf signaling upon bmp2b transcription. In transplantation experiments, we find that dorsalized cells from prospective ventrolateral regions of MZspg embryos are non cellautonomously respecified to a ventral fate within wild-type host embryos. Analysis of pou2 mRNA injected MZspg embryos shows that pou2 is required on the ventral side of cleavage stage embryos. Based on the maternal requirement for pou2 in ventral specification, we propose that ventral specification employs an active, pou2-dependent maternal induction step, rather than a default ventralizing program.

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“…They can also determine distinct morphogenetic behaviors (Bruce et al, 2005;Kwan and Kirschner, 2003;Russ et al, 2000;Yamomoto et al, 1998). T-box genes can be rapidly induced by growth factors, often in a dose-responsive manner (O'Reilly et al, 1995).…”

Section: T-box Genesmentioning

confidence: 99%

T-box transcription factors and their roles in regulatory hierarchies in the developing heart

2005

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T-box transcription factors are important players in the molecular circuitry that generates lineage diversity and form in the developing embryo. At least seven family members are expressed in the developing mammalian heart,and the human T-box genes TBX1 and TBX5 are mutated in cardiac congenital anomaly syndromes. Here, we review T-box gene function during mammalian heart development in the light of new insights into heart morphogenesis. We see for the first time how hierarchies of transcriptional activation and repression involving multiple T-box factors play out in three-dimensional space to establish the cardiac progenitors fields, to define their subservient lineages, and to generate heart form and function.

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T-box geneeomesoderminand the homeobox-containing Mix/Bix genemtx2regulate epiboly movements in the zebrafish

Cited by 47 publications

References 62 publications

The yolk syncytial layer regulates myocardial migration by influencing extracellular matrix assembly in zebrafish

The yolk syncytial layer regulates myocardial migration by influencing extracellular matrix assembly in zebrafish

Maternal control of vertebrate dorsoventral axis formation and epiboly by the POU domain protein Spg/Pou2/Oct4

T-box transcription factors and their roles in regulatory hierarchies in the developing heart

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