Congress Abstracts - Society for Developmental Biology

oligodendrocytes of the central nervous system. We have also observed possible estrogenic effects, which we are currently
investigating further. Thus, our research supports and expands on what is known about the effect of crude oil on the developing
embryo, and allows us to model what might have happened and will happen to native fish species in the Gulf.
Program/Abstract # 580
Isolation and Characterization of an ethanol sensitive zebrafish mutant
Lovely, Charles B. (UT- Austin, USA); Ackerman, Matt (U Indiana-Bloomington, USA); Henegar, Taylor (St. Edwards Univ, U SA);
Eberhart, Johann (UT-Austin, USA)
Fetal ethanol exposure causes a wide range of developmental defects that can include lower jaw hypoplasia. Cranial neural crest cells
generate much of the craniofacial skeleton, including the lower jaw. They migrate from the dorsal neural tube and condense in the
pharyngeal arches, where complex interactions between the neural crest cells and the adjacent epithelia are crucial in proper jaw
formation. While there is a greater understanding of effects of ethanol dosage and timing, little is known of the genetic predisposition
to ethanol-induced developmental defects. Using zebrafish, we performed a forward genetic screen to identify ethanol-sensitive
mutants, from which we recovered uta-15. Under control conditions, uta-15 embryos have no apparent craniofacial defects. Upon
exposure to 1% ethanol, 25% of embryos exhibit lower jaw hypoplasia. uta-15 embryos are most sensitive to ethanol between 24-48
hours post fertilization (hpf). By 32 hpf, the neural crest cells that generate the lower jaw have properly condensed into the pharyngeal
arches and no defects in endoderm morphology were apparent. At 36 hpf, expression of oral ectoderm markers was normal, as was
that of the ventral neural crest markers, hand2 and msxe. However, two neural crest markers necessary for proper lower jaw formation,
barx1 and nkx3.2, were misexpressed. In ethanol treated uta-15 embryos expression of barx1, which labels the prechondrogenic
condensations in the arches, was lost in the first pharyngeal arch and reduced in the subsequent arches. Additionally, nkx3.2, which
labels the jaw joint, appears reduced. Whole genome sequencing has identified a 20 Mbp interval on chromosome 14 that contains the
lesion and we are currently narrowing this interval. These data suggest a model where ethanol interacts with uta-15 altering the
expression of the specific neural crest markers necessary for proper lower jaw development. Overall, this work will provide greater
insight into gene-ethanol interactions and will allow for better diagnosis and treatment.
Program/Abstract # 581
High sucrose ingestion during the critical window of the pancreas modifies vascular contractility leading to metabolic
syndrome and hypertension in adult rats
Guarner, Veronica; Rubio-Ruiz, Maria Esther; Perez-Torres, Israel (Inst Nac de Cardiologia “Ignacio Chávez”, Mexico); Diaz-Diaz,
Eulises (Inst Nac de Ciencias Medicas y Nutricion "Salvador Zubiran”, Mexico)
Adverse conditions during early stages may permanently modify the function of the organism having consequences that are adaptive
in early life but may lead to metabolic syndrome (MS) in adult life. The effects of modified diets during early stages upon
susceptibility to hypertension in adults haven’t been studied. There is a critical period of pancreatic development (CPPD) in the rat
(postnatal days 12 to 28) with changes in plasma insulin and glucose. We study aortic vasoreactivity in rats during CPPD and compare
it to vasoreactivity in control and MS rats. We also study if high sucrose ingestion during CPPD modifies vascular contractility
leading to hypertension. Newborn male Wistar rats were divided into four groups: a) rats receiving sucrose 30% in drinking water
during CPPD, b) sucrose after CPPD until 6 months, c) sucrose during and after CPPD (MS rats), d) without sucrose. Glucose and
insulin were higher during suckling and decreased after weaning. NE induced contraction increased from day 12 to 21 but stabilized
form day 21 to day 28. Vaso-relaxation to acetylcholine didn’t change during the neonatal period. Changes were smaller than in MS
rats. Adult rats that had received sucrose during the critical window and after it had increased blood pressure as adults. NE-contraction
was similar to controls and relaxation was diminished. NO sinthase expression was increased while responses to endothelin receptor
blockers were not modified. In conclusion, there is a postnatal critical window in vaso-reactivity that accompanies that of the pancreas
and variations are smaller than in MS rats. A high sucrose diet during the critical window of the pancreas predisposes to the
development of hypertension in the adult.
Program/Abstract # 582
Pharmacological doses of biotin administered during the post-weaning period accelerate morphological and functional
development of pancreatic islet
Flores-Aguilar, Maura; Díaz-Martínez, Emmanuel; Fernández-Mejía, Cristina (UNAM, Mexico)
Biotin is a water-soluble vitamin that acts as a coenzyme of carboxylases. Unrelated to this role, pharmacological concentrations of
biotin has a wide repertoire of effects on syste mic processes such as development and carbohydrate metabolism. In previous studies
we found that after eight weeks of biotin supplementation in the diet increases the expression of genes regulating insulin synthesis,
also increases insulin secretion and augment the proportion of β cells. Furthermore in our studies the administration of the biotin
began in the weaning stage, a critical peri od in the islet development, we try to demonstrate if it is possible that the changes produced
by biotin supplementation observed at eight weeks of diet administration are carried out during post-weaning period. To test this
hypothesis, male BALB/cAnN Hsd mice were fed with control or a biotin-supplemented diet over seven days post-weaning (0.8 or
100 mg biotin/kg). At the end of treatment we found that the isolated islets from vitamin-supplemented mice presents glucosestimulated
insulin secretion due to an enhancement expression of the protein regulating glucose sensing (Glut2), whereas the control
group did not respond to stimulation as usual in immature neonatal islet. Consistent with these effects, glucose and insulin tolerance
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