Department of Biology: Rodolfo Aramayo

3258 TAMU
College Station, TX 77843-3258

Office:
Biological Sciences Building West
Room 414A
979-862-4354

Lab:
Biological Sciences Building West
Room 415
979-862-4376

Fax: 979-845-2891
Email: raramayo@tamu.edu

Biography

Rodolfo Aramayo joined the Department of Biology faculty at Texas A&M University in September of 1997. He is an Associate Professor of Biology and a member of the Interdisciplinary Faculty of Genetics at Texas A&M University in College Station, Texas. He is currently also an Associate Editor of PLoS ONE, The International Journal of Biological Sciences, Open Mycology and Fungal Genetics Reports.

His fields of expertise include molecular biology, genetics, epigenetics, genomics, chromosome biology, meiosis, RNA silencing, fungal developmental biology, bioinformatics and evolution. He teaches Genomics, Epigenetics and Chromosome Biology, all at graduate and undergraduate levels.

He earned a BSc and an MSc, both in Molecular Biology, from the University of Brasília (Brasília, Brazil). He obtained a PhD in Genetics under the direction of Dr. William E. Timberlake at the University of Georgia (Athens, Georgia), and held postdoctoral positions at the University of Wisconsin in Madison and Stanford University, both under the supervision of Dr. Robert L. Metzenberg.

His PhD research was centered on understanding the molecular mechanisms controlling the activation of developmental genes at specific times and places during conidiophore formation in Aspergillus nidulans. During his postdoctoral studies, he uncovered a novel genome defense mechanism, meiotic silencing, that not only is active in the meiotic cells of Neurospora crassa, but that of other organisms as well. During meiosis, the machinery involved in meiotic silencing evaluates the level of similarity of homologous chromosomes. If differences are found, such as those that would be the result of the insertion of transposable elements in one of the participating genomes in the cross, meiotic silencing promptly silences the expression of all transcripts that might be encoded by the loop of unpaired DNA and that of those homologous sequences that might be located elsewhere, even if they are paired. Meiotic silencing is therefore a unique and a very efficient mechanism of genome defense. In addition, because mutants in meiotic silencing greatly increase the fertility of interspecific crosses, he thinks meiotic silencing also plays an important role in the maintenance of reproductive isolation.

Genetics, Epigenetics and Meiotic RNA Silencing

In my laboratory, we use the filamentous fungus Neurospora crassa, as a model organism to understand meiotic silencing, one of the most amazing and intriguing mechanism observed in meiotic cells of eukaryotic organisms. If a segment of DNA is not present on the opposite homologous chromosome in meiosis in Neurospora, the resulting "unpaired" DNA segment is targeted for silencing. This situation occurs when a DNA element gets inserted at a particular chromosomal position (e.g., a situation akin to the "invasion" of a genome by transposable DNA elements). It can also occur when a normal region gets deleted. In both situations, the resulting loop of "unpaired" DNA activates a genome-wide "alert" system that results in the silencing not only of the genes present in the "unpaired" DNA segment, but also of those same genes if present elsewhere in the genome, even if they are in the paired condition. This phenomenon is called, meiotic silencing and was originally described in Neurospora crassa, but has since been observed in nematodes and mammals. In all these organisms, "unpaired or unsynapsed" regions (or chromosomes) are targeted for gene silencing. We think that meiotic silencing is a two-step process. First meiotic trans-sensing compares the chromosomes from each parent and identifies significant differences as unpaired DNA. Second, if unpaired DNA is identified, a process called meiotic silencing silences expression of genes within the unpaired region and regions sharing sequence identity. We are using a combination of genetics, molecular biology and biochemistry aimed at identifying all the molecular players of the process and at understanding how they work together. Our work is centered on understanding the genetic, molecular, cytogenetic and biochemical characterization of key components of the system: Sms-2, Sms-3, Sms-4, Sms-5, Sms-6, Sms-7, Sms-8, Sms-9, Sms-10 and Sms-11. The long term objective of our work is to understand meiotic silencing in Neurospora and to map its connections with the meiotic silencing observed in other organisms.

Selected Publications

Ng DW, Wang T, Chandrasekharan MB, Aramayo R, Kertbundit S, et al. (2007) Plant SET domain-containing proteins: structure, function and regulation. Biochim Biophys Acta 1769: 316-329.

Kelly WG, Aramayo R (2007) Meiotic silencing and the epigenetics of sex. Chromosome Res 15: 633-651.

Pratt RJ, Lee DW, Aramayo R (2004) DNA Methylation Affects Meiotic trans-sensing, Not Meiotic Silencing, in Neurospora. Genetics 168: 1925-1935.

Lee DW, Seong K-Y, Pratt RJ, Baker K, Aramayo R (2004) Properties of Unpaired DNA Required For Efficient Silencing in Neurospora crassa. Genetics 167: 131-150.

Freitag M, Lee DW, Kothe GO, Pratt RJ, Aramayo R, et al. (2004) DNA methylation is independent of RNA interference in Neurospora. Science 304: 1939.

Borkovich KA, Alex LA, Yarden O, Freitag M, Turner GE, et al. (2004) Lessons from the genome sequence of Neurospora crassa: tracing the path from genomic blueprint to multicellular organism. Microbiology and Molecular Biology Reviews 68: 1-108, table of contents.

Lee DW, Pratt RJ, McLaughlin M, Aramayo R (2003) An argonaute-like protein is required for meiotic silencing. Genetics 164: 821-828.

Lee DW, Haag JR, Aramayo R (2003) Construction of strains for rapid homokaryon purification after integration of constructs at the histidine-3 (his-3) locus of Neurospora crassa. Current Genetics 43: 17-23.

Kutil BL, Seong KY, Aramayo R (2003) Unpaired genes do not silence their paired neighbors. Current Genetics 43: 425-432.

Haag JR, Lee DW, Aramayo R (2003) A GATEWAY™ destination vector for high-throughput construction of Neurospora crassa histidine-3 gene replacement plasmids. Fungal Genetics Newsletter 50: 6-8.

Haag JR, Aramayo R (2003) Construction of a his-3 integration vector capable of performing GATEWAY recombinational cloning for high-throughput analysis of Neurospora crassa. Fungal Genetics Newsletter 50: 6-8.

Galagan JE, Calvo SE, Borkovich KA, Selker EU, Read ND, et al. (2003) The genome sequence of the filamentous fungus Neurospora crassa. Nature 422: 859-868.

Pratt RJ, Aramayo R (2002) Improving the efficiency of gene replacements in Neurospora crassa: a first step towards a large-scale functional genomics project. Fungal Genetics and Biology 37: 56-71.

Aramayo R, Peleg Y, Addison R, Metzenberg R (1996) Asm-1+, a Neurospora crassa gene related to transcriptional regulators of fungal development. Genetics 144: 991-1003.

Aramayo R, Metzenberg RL (1996) Meiotic transvection in fungi. Cell 86: 103-113.

 

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