Mason DA et al. (2009) J Mol Evol "Evolution of the metazoan-specific importin alpha gene family."

Stage DE, Mason DA, Goldfarb DS

[J Mol Evol, 2009]

Importin alphas are import receptors for nuclear localization signal-containing proteins. Most animal importin alphas assort into alpha1, alpha2, and alpha3 groups. Studies in Drosophila melanogaster, Caenorhabditis elegans, and mouse suggest that the animal importin alpha gene family evolved from ancestral plant-like genes to serve paralog-specific roles in gametogenesis. To explore this hypothesis we extended the phylogenetic analysis of the importin alpha gene family to nonbilateral animals and investigated whether animal-like genes occur in premetazoan taxa. Maximum likelihood analysis suggests that animal-like importin alpha genes occur in the Choanoflaggelate Monosiga brevicollis and the amoebozoan Dictyostelium; however, both of these results are caused by long-branch attraction effects. The absence of animal-like alpha genes in premetazoan taxa is consistent with the hypothesis that they duplicated and then specialized to function in animal gametogenesis. The gene structures of the importin alphas provide insight into how the animal importin alpha gene family may have evolved from the most likely ancestral gene. Interestingly, animal alpha1s are more similar to plant and fungal alpha1-like sequences than they are to animal alpha2s or alpha3s. We show that animal alpha1 genes share most of their introns with plant alpha1-like genes, and alpha2s and alpha3s share many more intron positions with each other than with the alpha1s. Together, phylogenetics and gene structure analysis suggests a parsimonious path for the evolution of the mammalian importin alpha gene family from an ancestral alpha1-like progenitor. Finally, these results establish a rational basis for a unified nomenclature of the importin alpha gene family.

Mason DA et al. (2008) Development "dmd-3, a doublesex-related gene regulated by tra-1, governs sex-specific morphogenesis in C. elegans."

Rabinowitz JS, Mason DA, Portman DS

[Development, 2008]

Although sexual dimorphism is ubiquitous in animals, the means by which sex determination mechanisms trigger specific modifications to shared structures is not well understood. In C. elegans, tail tip morphology is highly dimorphic: whereas hermaphrodites have a whip-like, tapered tail tip, the male tail is blunt-ended and round. Here we show that the male-specific cell fusion and retraction that generate the adult tail are controlled by the previously undescribed doublesex-related DM gene dmd-3, with a secondary contribution from the paralogous gene mab-3. In dmd-3 mutants, cell fusion and retraction in the male tail tip are severely defective, while in mab-3; dmd-3 double mutants, these processes are completely absent. Conversely, expression of dmd-3 in the hermaphrodite tail tip is sufficient to trigger fusion and retraction. The master sexual regulator tra-1 normally represses dmd-3 expression in the hermaphrodite tail tip, accounting for the sexual specificity of tail tip morphogenesis. Temporal cues control the timing of tail remodeling in males by regulating dmd-3 expression, and Wnt signaling promotes this process by maintaining and enhancing dmd-3 expression in the tail tip. Downstream, dmd-3 and mab-3 regulate effectors of morphogenesis including the cell fusion gene eff-1. Together, our results reveal a regulatory network for male tail morphogenesis in which dmd-3 and mab-3 together occupy the central node. These findings indicate that an important conserved function of DM genes is to link the general sex determination hierarchy to specific effectors of differentiation and morphogenesis.

Monoson HL et al. (1973) Mycopathologia et Mycologia Applicata "Endoparasitic nematode-trapping fungi of Mason State Forest."

Monoson HL, Williams SA

[Mycopathologia et Mycologia Applicata, 1973]

An initial survey involving the endoparasitic nematode-trapping fungi of Mason State Forest in Illinois was conducted from 15 May to 26 July 1971. Three endoparasitic forms were isolated from the soil samples collected; one non-endoparasitic form was also isolated. Soil pH's and soil nutrient levels were determined for the investigation period.

Harris TW et al. (2000) J Cell Biol "Mutations in synaptojanin disrupt synaptic vesicle recycling."

Harris TW, Hartweig EA, Jorgensen EM, Horvitz HR

[J Cell Biol, 2000]

Synaptojanin is a polyphosphoinositide phosphatase that is found at synapses and binds to proteins implicated in endocytosis. For these reasons, it has been proposed that synaptojanin is involved in the recycling of synaptic vesicles. Here, we demonstrate that the unc-26 gene encodes the Caenorhabditis elegans ortholog of synaptojanin. unc-26 mutants exhibit defects in vesicle trafficking in several tissues, but most defects are found at synaptic termini. Specifically, we observed defects in the budding of synaptic vesicles from the plasma membrane, in the uncoating of vesicles after fission, in the recovery of vesicles from endosomes, and in the tethering of vesicles to the cytoskeleton. Thus, these results confirm studies of the mouse synaptojanin 1 mutants, which exhibit defects in the uncoating of synaptic vesicles (Cremona, O., G. Di Paolo, M.R. Wenk, A. Luthi, W.T. Kim, K. Takei, L. Daniell, Y. Nemoto, S.B. Shears, R.A. Flavell, D.A. McCormick, and P. De Camilli. 1999. Cell. 99:179-188), and further demonstrate that synaptojanin facilitates multiple steps of synaptic vesicle recycling.