Dr. Adam Mason
Office: 013 Morrell Science Center
B.S. Biology, SUNY Geneseo (1995)
Ph.D. Biology, University of Rochester (2003)
Postdoctoral Studies at University of Rochester (2003-2005) and University of Rochester Medical Center (2005-2008)
Biol 110 - General Biology I and Biol 120 - General Biology II
Biol 190 - Writing and Research Skills for Biologists
Biol 345 – Developmental Genetics
Nearly all animal species generate two morphologically distinct sexes. The upstream cell signaling events dictating sexual identity have been well studied in many model organisms as well as in humans. In contrast, the mechanisms by which sex-determination signaling pathways alter developmental and cell biological processes are just beginning to be explored. To address this issue I study the cell biological, developmental and genetic processes that generate sex-differences in the small soil worm C. elegans, a powerful genetic model organism.
C. elegans has two sexes, males and hermaphrodites, that are different for a number of traits. The sex of C. elegans is controlled by the sex chromosomes; XX = hermaphrodites (essentially females that produce a small number of sperm) and XO = males. A complex genetic pathway interprets the sex chromosome ratio and dictates the sex of the entire organism. This pathway results in the selective activation of TRA-1, a regulator of gene expression, only in the hermaphrodite. TRA-1 in turn controls the activity of multiple differentiation pathways, each of which controls one component of sex-specific development. TRA-1 accomplishes this by repressing the expression of a handful of master regulators of male-specific differentiation. These master regulators influence developmental and cell biological processes to create sex-differences in body morphology / function. While much is known about how TRA-1 is activated only in hermaphrodites, only a subset of master regulators of male-specific differentiation have been identified.
I have identified a conserved gene, named DMD-3, that functions as the master regulator of sex-differences in tail tip morphology. The hermaphrodite adult tail tip is long and pointed, while the male tail tip is blunt ended (Figure 1A). These sex-differences are generated by a complex remodeling process that occurs only in males during the last larval mold (Figure 1B). Four pieces of evidence support the hypothesis that DMD-3 is the master regulator of morphogenesis
1. Males lacking DMD-3 function display a feminized pointed tail tip. (Figure 1C)
2. DMD-3 is expressed in the male tail tip coincident with tail remodeling (Figure 1D)
3. Mutating a conserved TRA-1 binding site in the DMD-3 promoter results in expression in the hermaphrodite tail tip, presumably due to the loss of TRA-1 inhibition (not shown).
4. Expression of DMD-3 in the hermaphrodite tail tip is sufficient to induce remodeling in a location in which it normally never occurs (not shown).
1. Characterize the role of dmd-3 and the closely related gene, mab-3, in regulating multiple aspects of male-specific development. As can be seen in Figure 1D dmd-3 is expressed male specifically in a number of tissues. Notably all of these tissues undergo male-specific development. I am currently examining the function of dmd-3 in mediating these male-specific processes. For example, dmd-3 is strongly expressed in the linker cell, a male-specific cell that leads the migration of the male gonad down to the tail region. Preliminary data suggests that dmd-3 functions together with mab-3 to mediate the development the linker cell. In dmd-3 ; mab-3 double mutant males the linker cell does not migrate properly and often does not die at the correct time. We are performing experiments to further characterize these defects and to determine the mechanisms by which dmd-3 and mab-3 control linker cell development. In addition, we are performing experiments to determine how dmd-3 controls the complex developmental process of anterior tail retraction.
2. Characterize the cell biological changes that occur within the four tail tip cells during tail tip retraction. Tail tip retraction is a relatively simple remodeling process involving only four cells. Therefore, this process can serve as a good model for understanding similar, but more complex, processes that occur during human development. Despite this simplicity very little is known about the changes in the cell biology of these cells during remodeling. Using a battery of fluorescently labeled transgenes I will be examining the changes in the cytoskeleton, vesicle transport, expression of cell adhesion molecules, cell fusion and cell shape that occurs during male-specific tail tip remodeling. After the initial characterization of the cell biology of these cells I will examine how DMD-3 controls each of these changes.
I believe that an important role of my research is to encourage and train undergraduate students to design and perform novel experiments. For this reason I aim to have approximately 4-6 undergraduate research students working in my lab at all times. If you are interested in performing research with me I would encourage you to take a look a recent publication to get a feel for the types of experiments that I do in my lab. Contact me by email (email@example.com) or stop by my office (MSC013) to inquire about performing research with me.
I teach one lecture section and two lab sections of General Biology I and II (Biol. 110 & 120) during the Fall and Spring semesters. Biol110 gives an overview of topics in cell biology, genetics and evolution while Biol120 covers the diversity of life with an emphasis on how diverse life forms affect human health. I also teach a section of Writing and Research Skills for Biologists. This course teaches students how to design and perform experiments, interpret data and present your results in the form of a scientific paper. Finally, I teach Biol 345 – Developmental Genetics. This course examines the genetic and cellular control of animal developmental processes. This course includes a lab component that highlights genetic techniques utilized in the major model organisms (the nematode C. elegans, the fruit fly Drosophila melanogaster, the snail Ilyanassa, the fish Danio rerio and sea urchins).
Mason, D.A., Rabinowitz, J.S. and D.S. Portman. 2008. dmd-3, a doublesex-related gene regulated by tra-1, governs sex-specific morphogenesis in C. elegans. Development, 135: 2373-2382. Full text PDF. Selected as a Faculty of 1000 must-read paper.
Mason, D.A. Stage, D., and D.S. Goldfarb. 2009. Evolution of the metazoan-specific importin alpha gene family. J Mol Evol. 68:351-365. Full Text PDF.
Ratan, R.*, Mason, D.A.*, Sinnott, B., Goldfarb, D.S. and R.J. Fleming. 2008. Drosophila importin alpha1 performs paralog-specific functions essential for gametogenesis. Genetics, 178: 839-850. Full text PDF * Authors contributed equally to this work.
Mason, D.A., Shulga, N., Undavai, S., Ferrando-May, E., Rexach, M.F. and D.S. Goldfarb. 2005. Increased nuclear envelope permeability and Pep4p-dependent degradation of nucleoporins during hydrogen peroxide-induced cell death. FEMS Yeast Res., 5:1237-1251. Full text.
Mason D. A., Mathe, E., Fleming, R.J. and D.S. Goldfarb. 2003. The Drosophila melanogaster importin a3 locus encodes an essential gene required for the development of both larval and adult tissues. Genetics, 165: 1943-1958. Full text PDF
Mason, D.A., Fleming, R.J. and D.S. Goldfarb. 2002. Drosophila melanogaster importin a1 and a3 can replace importin a2 during spermatogenesis but not oogenesis. Genetics, 161:157-170. Full text PDF
Reviews / Bookchapters
Mason, D.A. and D.S. Goldfarb. 2009. The nuclear transport machinery as a regulator of Drosophila development. In D. Jans (Ed) Nuclear Transport in Development and Disease. Seminars in Cell and Developmental Biology. 20:582-589. Full text.
Goldfarb, D.S., Corbett, A.H., Mason, D.A., Harreman, M.T., and S.A. Adam. 2004. Importin a: a multipurpose nuclear-transport receptor. Trends in Cell Biology, 14:505-514. Full text PDF.
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