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1.  The molecular basis of defective lens development in the Iberian mole 
BMC Biology  2008;6:44.
Fossorial mammals face natural selection pressures that differ from those acting on surface dwelling animals, and these may lead to reduced visual system development. We have studied eye development in a species of true mole, the Iberian mole Talpa occidentalis, and present the molecular basis of abnormal lens development. This is the first embryological developmental study of the eyes of any fossorial mammal at the molecular level.
Lens fibre differentiation is not completed in the Iberian mole. Although eye development starts normally (similar to other model species), defects are seen after closure of the lens vesicle. PAX6 is not down-regulated in developing lens fibre nuclei, as it is in other species, and there is ectopic expression of FOXE3, a putative downstream effector of PAX6, in some, but not all lens fibres. FOXE3-positive lens fibres continue to proliferate within the posterior compartment of the embryonic lens, but unlike in the mouse, no proliferation was detected anywhere in the postnatal mole lens. The undifferentiated status of the anterior epithelial cells was compromised, and most of them undergo apoptosis. Furthermore, β-crystallin and PROX1 expression patterns are abnormal and our data suggest that genes encoding β-crystallins are not directly regulated by PAX6, c-MAF and PROX1 in the Iberian mole, as they are in other model vertebrates.
In other model vertebrates, genetic pathways controlling lens development robustly compartmentalise the lens into a simple, undifferentiated, proliferative anterior epithelium, and quiescent, anuclear, terminally differentiated posterior lens fibres. These pathways are not as robust in the mole, and lead to loss of the anterior epithelial phenotype and only partial differentiation of the lens fibres, which continue to express 'epithelial' genes. Paradigms of genetic regulatory networks developed in other vertebrates appear not to hold true for the Iberian mole.
PMCID: PMC2587461  PMID: 18939978
2.  Video analysis of the escape flight of Pileated Woodpecker Dryocopus pileatus: does the Ivory-billed Woodpecker Campephilus principalis persist in continental North America? 
BMC Biology  2007;5:8.
The apparent rediscovery of the Ivory-billed Woodpecker Campephilus principalis in Arkansas, USA, previously feared extinct, was supported by video evidence of a single bird in flight (Fitzpatrick et al, Science 2005, 308:1460–1462). Plumage patterns and wingbeat frequency of the putative Ivory-billed Woodpecker were said to be incompatible with the only possible confusion species native to the area, the Pileated Woodpecker Dryocopus pileatus.
New video analysis of Pileated Woodpeckers in escape flights comparable to that of the putative Ivory-billed Woodpecker filmed in Arkansas shows that Pileated Woodpeckers can display a wingbeat frequency equivalent to that of the Arkansas bird during escape flight. The critical frames from the Arkansas video that were used to identify the bird as an Ivory-billed Woodpecker are shown to be equally, or more, compatible with the Pileated Woodpecker.
The identification of the bird filmed in Arkansas in April 2004 as an Ivory-billed Woodpecker is best regarded as unsafe. The similarities between the Arkansas bird and known Pileated Woodpeckers suggest that it was most likely a Pileated Woodpecker.
PMCID: PMC1838407  PMID: 17362504
3.  The roles of calcium signaling and ERK1/2 phosphorylation in a Pax6+/- mouse model of epithelial wound-healing delay 
BMC Biology  2006;4:27.
Congenital aniridia caused by heterozygousity at the PAX6 locus is associated with ocular surface disease including keratopathy. It is not clear whether the keratopathy is a direct result of reduced PAX6 gene dosage in the cornea itself, or due to recurrent corneal trauma secondary to defects such as dry eye caused by loss of PAX6 in other tissues. We investigated the hypothesis that reducing Pax6 gene dosage leads to corneal wound-healing defects. and assayed the immediate molecular responses to wounding in wild-type and mutant corneal epithelial cells.
Pax6+/- mouse corneal epithelia exhibited a 2-hour delay in their response to wounding, but subsequently the cells migrated normally to repair the wound. Both Pax6+/+ and Pax6+/- epithelia activated immediate wound-induced waves of intracellular calcium signaling. However, the intensity and speed of propagation of the calcium wave, mediated by release from intracellular stores, was reduced in Pax6+/- cells. Initiation and propagation of the calcium wave could be largely decoupled, and both phases of the calcium wave responses were required for wound healing. Wounded cells phosphorylated the extracellular signal-related kinases 1/2 (phospho-ERK1/2). ERK1/2 activation was shown to be required for rapid initiation of wound healing, but had only a minor effect on the rate of cell migration in a healing epithelial sheet. Addition of exogenous epidermal growth factor (EGF) to wounded Pax6+/- cells restored the calcium wave, increased ERK1/2 activation and restored the immediate healing response to wild-type levels.
The study links Pax6 deficiency to a previously overlooked wound-healing delay. It demonstrates that defective calcium signaling in Pax6+/- cells underlies this delay, and shows that it can be pharmacologically corrected. ERK1/2 phosphorylation is required for the rapid initiation of wound healing. A model is presented whereby minor abrasions, which are quickly healed in normal corneas, transiently persist in aniridic patients, compromising the corneal stroma.
PMCID: PMC1563477  PMID: 16914058

Results 1-3 (3)