Emily Beck and Juan Santana will present their research on February 16th, 2012

Background for Emily’s talk


Introgression is the exchange of genetic information between different species through natural hybridization.  Once viewed as a fortuitous accident due to incomplete reproductive isolation between species, it has become increasingly clear that introgression can potentially lead to ecological divergence, crop improvement or even invasiveness.  Recent molecular genetic studies in plants indicate that introgression may allow populations to regain traits that have been lost by replacing the damaged alleles with functional copies from a closely related species. Novelty can also arise from introgression.  Unique genetic combinations that result from the stable acquisition of genetic material from another species can produce new phenotypes and serve as source for novel adaptations.  Hybrid zones, areas where two distinct species meet and hybridize, provide biologists with natural experiments and thus constitute ideal settings to study introgression.  Unfortunately there is a dearth of hybrid zones in one of the most genetically well-studied group, Drosophila.  In 2000, however, a new unique hybrid zone formed by two species in the melanogaster subgroup, Drosophila yakuba and D. santomeawas discovered in a small African island of the Gulf of Guinea.  Previous studies in our lab showed that the mitochondrial genome of the former species had introgressed into the latter and replaced completely the native form.  Since mitochondrial DNA products work intimately with nuclear DNA products in the oxidative phosphorilation pathway (i.e. OXPHOS) that takes place in mitochondria, we hypothesize that some nuclear genes in OXPHOS co-introgressed along with the mitochondrial genome.  To test this hypothesis we have sequenced 12 genes of the OXPHOS pathway in a total of 33 Drosophila lines.  Our preliminary results suggest that co-introgression has indeed occurred and support the idea of co-evolution between both mitochondrial and nuclear genomes.

Background for Juan’s talk

Drosophila Myb interacts with NURF to repress cell cycle genes and transposons in non-mitotic tissues

c-Myb is encoded by a proto-oncogene associated with leukemias and lymphomas in birds and mammals. Vertebrates have three representatives of the Myb gene family consisting of A-, B- and c-Myb, all of which encode DNA-binding factors that are important for the proper expression of large numbers of genes including those that regulate cell cycle progression and cell differentiation. Drosophila melanogastercontains a single Myb gene (Dm-Myb), mutants of which die before reaching adulthood.  siRNA knockdown of Dm-Myb was shown to reduce expression of genes with prominent roles in coordinating cell division in an embryonic Drosophila cell line.  Along the same lines, Dm-Myb mutant flies display cell cycle defects such as aneuploidy and polyploidy, both hallmarks of cancer. Additionally, the Dm-Myb protein was identified in a complex containing a large number of proteins including the nucleosome remodeling factor NURF. Through yeast two-hybrid and genetic screens, we have now established that DmMyb specifically interacts with the major subunit of NURF (Nurf301).  In light of these results, we performed gene expression analyses in Dm-Myb and Nurf301 mutant animals under the assumption that a significant number of genes are co-regulated by both proteins. As expected but nonetheless striking, there is an almost 50% overlap of the genes regulated by these two proteins and, in contrast to the dogma in the field, we have observed a prominent transcriptional repression function for Myb and Nurf301 in non-mitotic tissues. These data suggest that, in addition to activation of cell cycle genes in dividing cells, Myb and NURF work to repress such genes in non-dividing cells. Even more surprising, tiling microarray and RNA-seq data indicate that Dm-Myb and Nurf301 are working in concert to silence transposable elements.


Posted on February 9, 2012, in Student Seminar. Bookmark the permalink. Leave a comment.

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