Given that some of the phenotypes associated with RTT could be attributed to hypothalamic dysfunction, Chahrour et al. (2008) defined the hypothalamic gene profile of WT, MeCP2-null and MeCP2-overexpressing (MeCP2-tg) mice using microarray screening.
That the Dutch were so quick off the mark with manipulations such as mammalian RNA inhibition, conditional mouse knockouts, and vast microarray screens could, at least in part, be due to this propensity to be open-minded and to take risks.
To assess the relative importance of each cell type and the potential overlap with mouse gonadal expression profiles we compared our screen and three high throughput microarray screens carried out on embryonic mouse gonads/cells at a similar stage of differentiation [ 32– 32].
There is good agreement between the genes highlighted by our in-silico binding-site search and by microarray screens for downstream targets of hoxb1 in rhombomere 4 of zebrafish [ 52] and mouse [ 53].
We currently produce DNA microarrays representing the yeast, mouse, and human genomes (the yeast microarray has over 6000 yeast genes, the mouse microarray has over 15,000 mouse genes, and the two human microarrays have 1700 genes and over 19,000 genes).
The microarray screens were conducted at the DNA Microarray facility of UCLA, Los Angeles.
Microarray screens published in the biomedical literature were additionally included in the c2 gene set.
Microarray screens for upstream regulators of cVg1.
Out of 743 human, rat and mouse miRNAs included on the microarray screen, we detected average upregulation (>1.75-fold) after ZEB1 knockdown of 79 miRNAs (10.59%) in at least one cell line, 17 miRNAs (2.27%) in two cell lines and only 4 miRNAs (0.53%) in all three cell lines (Fig 1; supplementary Table 1 online).
To test whether this regulation is specific for DBA/2J mice, or may also occur in C57BL/6J mice (but was not detected in our microarray screening, because of the selection filtering), we also tested the respective samples from C57BL/6J mice.
