High impact information on flh

• We propose that flh regulates notochord precursor cell fate [1].
• This is in contrast to zebrafish embryos, in which flh interacts with ntl (zebrafish T) in a regulatory loop and is essential for development of the entire notochord, and suggests that different genetic control circuits act in different vertebrate species during notochord formation [2].
• We show that mbl is required to prevent the expression of flh in dorsal forebrain cells rostral to the epiphysis [3].
• In flh- embryos, the first few epiphysial neurons are generated, but beyond the 18 somite stage, neuronal production ceases [3].
• In addition, a dominant-negative construct and antisense morpholino oligonucleotides led to a reduction in gsc and flh expression [4].

Biological context of flh

• In a large scale screen for mutants with defects in the embryonic development of the zebrafish we identified mutations in four genes,floating head (flh), momo (mom), no tail (ntl), and doc, that are required for early notochord formation [5].
• The borders of the notochord domain are sharp at the level of single cells, and coincide almost exactly with the border of the expression domain of the homeobox gene floating head (flh; zebrafish homologue of Xnot), a gene essential for notochord development [6].
• Here we demonstrate that bacterial artificial chromosomes can rescue the phenotype of floating head (flh) mutants [7].
• In contrast, control mutant embryos injected with artificial chromosomes lacking the flh+ gene failed to form notochord [7].

Anatomical context of flh

• The homeodomain transcription factor Floating head (Flh) is required for the generation of neurones in the zebrafish epiphysis [8].
• The midline mutants floating head (flh), sonic you (syu), and you-too (yot) provide the opportunity to study glomerular differentiation in the absence of the notochord and vascularization from the dorsal aorta [9].
• In flh mutants, cells in the notochord domain generate clones of muscle cells [6].
• A minority of cells in the notochord domain in wild-type embryos develop as unrestricted mesoderm, invariably located in the tail, suggesting that early gastrula expression of flh does not restrict cellular potential to the notochord fate [6].
• In ntl mutants the spatial pattern of flh expression is altered as early as the late gastrula stage, becoming broad and diffuse [10].

Regulatory relationships of flh

• In these mosaic embryos flh cells expressing flk assemble at the midline, beneath the wild-type notochord, and form an aortic primordium [11].
• Expression of hsp90alpha is also activated in the midline of flh mutants when these cells switch from a notochord to a muscle fate [12].
• floating head and masterblind regulate neuronal patterning in the roof of the forebrain [3].

Other interactions of flh

• We show that ash1a and ngn1 function in parallel redundant pathways to regulate neurogenesis downstream of flh [8].
• In contrast, the timing and morphology of otic development is not affected by mutations in no tail (ntl) or floating head (flh), which prevent notochord differentiation [13].

References