Papis E et al. (2007), Gene expression in Xenopus laevis embryos after...

XB-ART-89

Gene Expr Patterns 2007 Jan 01;71-2:137-42. doi: 10.1016/j.modgep.2006.06.003.

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Gene expression in Xenopus laevis embryos after Triadimefon exposure.

Papis E , Bernardini G , Gornati R , Menegola E , Prati M .

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The triazole derivative Triadimefon (FON) is a systemic fungicide used to control powdery mildews, rusts, and other fungal pests. Some data have already been published about the teratogenic activity of this compound: craniofacial malformations were found in mouse, rat, and Xenopus laevis embryos exposed to FON. These alterations were correlated to defective branchial arch development possibly caused by abnormal neural crest cell (NCC) migration into the branchial mesenchyme. As the migration of NCCs is controlled by the HOX code and by an anteroposterior retinoic acid (RA) gradient, we analyzed the expression of CYP26, a key enzyme in RA metabolism, following FON exposure. The increased expression of this gene and the ability of citral (a RA inhibitor) to reduce the teratogenic effects of the fungicide support the notion that endogenous RA is involved in the mechanism of action of FON. Moreover, by in situ hybridization, we studied the effects of FON exposure at gastrula stage on the expression of some genes involved in craniofacial development, hindbrain patterning, and NCC migration. We observed abnormal localization of xCRABP, Hoxa2 and Xbap signal expression at the level of migrating NCC domains, whereas in the hindbrain, we did not find any alteration in Krox20 and Hoxa2 expression.

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Species referenced: Xenopus laevis
Genes referenced: crabp1 crabp2 cyp26a1 egr2 hoxa2 nkx3-2 slc12a3

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	Fig. 2. Whole-mount in situ hybridization analysis of CYP26 expression in control (C) and gastrula-exposed (T) embryos at stage 27 (a) and 37 (b). The treated embryos show an increase in the expression signal intensity compared to controls. Note that the stage 37-exposed embryos showed a persistence of CYP26 signal at the level of branchial arches.
	Fig. 4. Whole-mount in situ hybridization analysis of xCRABP expression in control (C) and gastrula-exposed (T) embryos at stage 27. Note in the FON-exposed sample the presence of the expression signal at the level of the first and second branchial arch territories, which are normally devoid of xCRABP (white arrowhead).
	Fig. 5. Whole-mount in situ hybridization analysis of Hoxa2 expression in control (C) and gastrula-exposed (T) embryos at stage 22 (a,b), 27 (c), and 37 (d). No difference in Hoxa2 expression is shown at the level of hindbrain (b) while alterations are present at the level of migrating NCC domain (white arrowhead).
	Fig. 6. Whole-mount in situ hybridization analysis of Xbap [nkx3.2] expression in control (C) and gastrula-exposed (T) embryos at stage 37. Note in the treated sample a selective loss of Xbap expression at the level of the precursor of palatoquadrate and proximal part of Meckel’s cartilages (white arrowhead).
	Fig. 7. Whole-mount in situ hybridization analysis of Krox20 expression in control (C) and gastrula-exposed (T) embryos at stage 27. Alternating domains of Krox20 expression, corresponding to rhombomeres r3 and r5, are present both in control and treated specimens.