High impact information on tcf2

• The different requirements for vhnf1 and val to repress hoxb1a and ephrin-B2a, respectively, demonstrate that not all aspects of an individual rhombomere's identity are regulated coordinately [1].
• However, vhnf1 is not able to repress all aspects of r4 identity equivalently. val is required downstream of vhnf1 to repress r4-like cell-surface properties, as determined by an 'Eph-ephrin code', by repressing ephrin-B2a expression in r5 and r6 [1].
• We show that RA induces val expression via activation of vhnf1 expression in the hindbrain [1].
• We demonstrate that Iro7 represses vhnf1 expression anterior to their common border and that, conversely, vHnf1 represses iro7 expression caudal to it [2].
• This territory is strictly complementary to the expression domain of another homeobox gene, vhnf1, in the caudal neural plate [2].

Biological context of tcf2

• Forced expression of either hnf-6 or vhnf1 also produces biliary phenotypes [3].

Anatomical context of tcf2

• Recent work in the zebrafish has shown a requirement for fibroblast growth factor (Fgf) signaling and for the transcription factor variant hepatocyte nuclear factor 1 (vhnf1) in specification of rhombomeres 5 and 6 (r5+r6) [4].
• We show that early zebrafish rhombomere-specification genes, including vhnf1 in r5-r6 and hoxd4a in r7, initiate expression sequentially in the hindbrain, each adjacent to the source of RA synthesis in paraxial mesoderm [5].

Other interactions of tcf2

• We show here that vhnf1 functions in two ways to subdivide the zebrafish caudal hindbrain domain (r4-r7) into individual rhombomeres [4].
• Paralog group 1 hox genes regulate rhombomere 5/6 expression of vhnf1, a repressor of rostral hindbrain fates, in a meis-dependent manner [6].

References