foxi1 expression, increased leads to six1b expression, increased

Foxi1 is an early inducer of the otic placode and  positively regulates the expression of six1b transcription factor.

• When foxi1 is knocked down, the ear anlagen is either entirely missing or greatly reduced (Solomon et al., 2003) and no expression of six1b is detectable in otocyst. Because, at 28 hpf, the lack of six1b expression could be secondary to the overall absence of the otic placode attributable to foxi1 loss-of-function, six1b expression was studied at either 28 hpf in embryos with less severe phenotype or at 16.5 hpf when the placode just arises. In both cases, no expression of six1b was detected (Bricaud et al., 2006).
• Overexpression of six1b during inner development was achieved by injecting a synthetic six1b mRNA at early stages. Such gain-of- function experiments gave the opposite phenotype to that seen after six1b loss-of-function. At 3 dpf, more hair cells are present. This overproduction of hair cells is detectable as early as 28 hpf, with an average of four hair cells observed instead of the two in wild-type embryos. (Bricaud et al., 2006) assayed for the presence of differentiated neurons at 3 dpf and neural precursors at 32 hpf with the neuronal markers HuC and neuroD, respectively. At 32 hpf in the six1b overexpressing embryos, fewer neuroD positive cells are detectable in the otic ganglion than in control embryos, suggesting that fewer neural progenitors are formed when six1b is overexpressed. At 3 dpf, the decrease in number of SAG neurons versus controls is even more dramatic. In extreme cases, SAG neurons are completely eliminated. These results indicate that, when six1b is overexpressed, not only are fewer neural progenitors formed but many ofthese progenitors do not go on to differentiate into neurons. In conclusion, these, together with the six1b loss-of-function results, suggest that six1b is necessary and sufficient for the normal formation of hair cells in the anterior macula, although it inhibits neuronal fate in the developing inner ear.

No Data.

Foxi1 gene is critical for zebrafish otic induction (Solomon et al., 2003), while it is not essential for this process in mice (Hulander et al., 2003).

No Data.

• Expression of zebrafish six1b in the Inner Ear and Neuromasts: Expression of six1b was observed in the developing inner ear and neuromasts of the lateral line until 96 hpf, the latest stage analyzed in this study. Transcripts of six1b were detected in all five sensory patches of the inner ear as well as in the semicircular canals. Detected first at 48 hpf, six1b expression in neuromasts of the midbody lateral line reached its peak at 72 hpf  with stronger staining at the basal region of the neuromast, where bodies of hair cells are localized (Webb & Shirey, 2003).
• Expression of zebrafish six1b in Muscles: Since the beginning of segmentation six1b was expressed in the somites. At 72 hpf, the expression of six1b became more pronounced in the ventral somites with stronger staining in the most ventral cells. It continued in the pectoral fin and ventral abdomen muscle. Six1b expression was also found in the muscles of the eye and the lower jaw. (Bricaud et al., 2006).
• Temporal changes in gene expression and the emergence of sensory placode progenitors. As development proceeds gene expression domains sharpen through mutually repressive interactions; in the head region, the neural crest and placode precursor specific transcripts begin to be expressed at early neurula stages. Initially their boundaries are fuzzy, but gene expression resolves to distinct domains by late neurula (black dashed lines). NP: neural plate; NC: neural crest; PPR: preplacodal region; Epi: future epidermis. Right: diagram of an embryo at early neurula stages; dashed lines indicate the medial boundaries of non-neural transcripts (Lleras-Forero & Streit, 2012).

No Data.