To obtain an understanding of the relationships of the basidiomycetes, especially those with hori... more To obtain an understanding of the relationships of the basidiomycetes, especially those with horizontally partitioned metabasidia, and of the evolution of structural characters, members of nine orders and an additional four genera of simple-septate fungi (Auriculariales sensu lato) were studied using cladistic analysis of light microscopic and ultrastructural characters. Comparisons were made with the nucleotide sequence from the 5′ end of the nuclear large subunit ribosomal RNA gene analyzed with several algorithms, including parsimony and maximum likelihood. Analyses of both morphological and molecular characters support similar phylogenetic conclusions, but polarization of some morphological characters was difficult without guidance from molecular data. The Uredinales are shown to be an advanced taxon arising from the simple-septate Auriculariales sensu lato, and some characters that they share with the ascomycetes result from convergent evolution. The simple-septate Auricularial...
Prenatal alcohol exposure (PAE) causes distinctive facial characteristics in some pregnancies and... more Prenatal alcohol exposure (PAE) causes distinctive facial characteristics in some pregnancies and not others; genetic factors may contribute to this differential vulnerability. Ethanol disrupts multiple events of neural crest development, including induction, survival, migration, and differentiation. Animal models and genomic approaches have substantially advanced our understanding of the mechanisms underlying these facial changes. PAE during gastrulation produces craniofacial changes corresponding with human fetal alcohol syndrome. These result because PAE reduces prechordal plate extension and suppresses sonic hedgehog, leading to holoprosencephaly and malpositioned facial primordia. Haploinsufficiency in sonic hedgehog signaling increases vulnerability to facial deficits and may influence some PAE pregnancies. In contrast, PAE during early neurogenesis produces facial hypoplasia, preceded by neural crest reductions due to significant apoptosis. Factors mediating this apoptosis include intracellular calcium mobilization, elevated reactive oxygen species, and loss of trophic support from β-catenin/calcium, sonic hedgehog, and mTOR signaling. Genome-wide SNP analysis links PDGFRA with facial outcomes in human PAE. Multiple genomic-level comparisons of ethanol-sensitive and - resistant early embryos, in both mouse and chick, independently identify common candidate genes that may potentially modify craniofacial vulnerability, including ribosomal proteins, proteosome, RNA splicing, and focal adhesion. In summary, research using animal models with genome-level differences in ethanol vulnerability, as well as targeted loss-and gain-of-function mutants, has clarified the mechanisms mediating craniofacial change in PAE. The findings additionally suggest that craniofacial deficits may represent a gene-ethanol interaction for some affected individuals. Genetic-level changes may prime individuals toward greater sensitivity or resistance to ethanol's neurotoxicity.
To obtain an understanding of the relationships of the basidiomycetes, especially those with hori... more To obtain an understanding of the relationships of the basidiomycetes, especially those with horizontally partitioned metabasidia, and of the evolution of structural characters, members of nine orders and an additional four genera of simple-septate fungi (Auriculariales sensu lato) were studied using cladistic analysis of light microscopic and ultrastructural characters. Comparisons were made with the nucleotide sequence from the 5′ end of the nuclear large subunit ribosomal RNA gene analyzed with several algorithms, including parsimony and maximum likelihood. Analyses of both morphological and molecular characters support similar phylogenetic conclusions, but polarization of some morphological characters was difficult without guidance from molecular data. The Uredinales are shown to be an advanced taxon arising from the simple-septate Auriculariales sensu lato, and some characters that they share with the ascomycetes result from convergent evolution. The simple-septate Auricularial...
Prenatal alcohol exposure (PAE) causes distinctive facial characteristics in some pregnancies and... more Prenatal alcohol exposure (PAE) causes distinctive facial characteristics in some pregnancies and not others; genetic factors may contribute to this differential vulnerability. Ethanol disrupts multiple events of neural crest development, including induction, survival, migration, and differentiation. Animal models and genomic approaches have substantially advanced our understanding of the mechanisms underlying these facial changes. PAE during gastrulation produces craniofacial changes corresponding with human fetal alcohol syndrome. These result because PAE reduces prechordal plate extension and suppresses sonic hedgehog, leading to holoprosencephaly and malpositioned facial primordia. Haploinsufficiency in sonic hedgehog signaling increases vulnerability to facial deficits and may influence some PAE pregnancies. In contrast, PAE during early neurogenesis produces facial hypoplasia, preceded by neural crest reductions due to significant apoptosis. Factors mediating this apoptosis include intracellular calcium mobilization, elevated reactive oxygen species, and loss of trophic support from β-catenin/calcium, sonic hedgehog, and mTOR signaling. Genome-wide SNP analysis links PDGFRA with facial outcomes in human PAE. Multiple genomic-level comparisons of ethanol-sensitive and - resistant early embryos, in both mouse and chick, independently identify common candidate genes that may potentially modify craniofacial vulnerability, including ribosomal proteins, proteosome, RNA splicing, and focal adhesion. In summary, research using animal models with genome-level differences in ethanol vulnerability, as well as targeted loss-and gain-of-function mutants, has clarified the mechanisms mediating craniofacial change in PAE. The findings additionally suggest that craniofacial deficits may represent a gene-ethanol interaction for some affected individuals. Genetic-level changes may prime individuals toward greater sensitivity or resistance to ethanol's neurotoxicity.
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