I am interested in studying the mechanism of mitotic failure in Dicer mutant vertebrate cells. Dicer, an RNaseIII enzyme, is an important component of RNA mediated silencing and its absence leads to loss of centromeric silencing, defects in stem cell differentiation, microRNA (miRNA) processing defects, loss of transcriptional gene silencing (TGS), and cell death. I use Dicer-/- DT40 cells (chicken B-cell lymphoma cell line), and human colorectal cancer cells HCT116 for my studies.

jaspreet.khurana@umassmed.edu

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birgit.koppetsch@umassmed.edu

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My research interest is DNA repair and mutagenesis. DNA repair mechanisms are the key factors in the maintenance of genome integrity and stability, therefore defects in these pathways can lead to genetic diseases and cancer. In a previous lab I studied the molecular mechanisms of cytotoxicity induced by certain anticancer drugs such as cisplatin and methylating agents using bacterial model.

Presently my research is focused towards understanding the developmental role of RNA interference via repeat associated siRNA (rasiRNA) in fruit flies. Recently it has been shown that defects in components of rasiRNA pathway such as aubergine and armitage trigger accumulation of germline specific gamma-H2Av foci characteristic of DNA double strand breaks (Klattenhoff C. et al. 2007). Genetic analysis of this phenomenon indicated that the nature of these breaks is different from those induced during meiosis. Therefore it was concluded that the key developmental function of rasiRNA could be to suppress DNA damage signaling in the germline. Currently I am trying to understand the relationship between DNA damage signaling and rasiRNA interference in the protection of germline genome integrity in Drosophila melanogaster.

anetta.nowosielska@umassmed.edu

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With over 20 years of experience in Drosophila labs, I serve as an extra pair of hands in several of the lab projects with a strong focus on Drosophila genetics.  I’m supporting ongoing projects by creating double and triple mutants, as well as recombinant and transgenic flies. In addition to fly pushing, I help with phenotypic analyses on mutant ovaries and embryos using confocal microscopy. At the bench I’ve been involved in cloning, expressing and purifying fusion proteins for antibody production.  I’m responsible for maintaining the lab fly stocks and I assist in daily maintenance of the lab.

nadine.schultz@umassmed.edu

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Under normal conditions, the G2/M damage checkpoint delays progression into mitosis to allow time for repair.  However, when checkpoint control fails and cells enter mitosis with DNA lesions, mitosis is aborted through a poorly understood process termed mitotic catastrophe. Drosophila syncytial embryos are ideal to assay the mitotic DNA damage response, since they readily enter mitosis in the presence of damage. However, the long term goal of studying the mitotic DNA damage response will be to understand this process in humans, where it might be a tumour suppressing response that serves to eliminate damaged cells with a checkpoint deficient genetic background. Taking advantage of both model systems, I am addressing which mechanisms cells use to abort mitosis in response to DNA lesions.

Before joining Bill's lab in 2004, I studied centrosome function during spindle assembly in Drosophila (EMBL, Germany, 1999-2004) and worked on proteome profiling of human bladder tumours (University of Aarhus, Denmark, 1997-1999).

hanne.varmark @umassmed.edu

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In Drosophila melanogaster, piRNAs (piwi-interacting RNAs) are required to silence transposable elements.  However, the details of the silencing mechanism are unclear.  The long-term goal of my project is to determine the mechanism of piRNA-mediated silencing of transposable elements in Drosophila.  The fact that piRNAs show substantial sequence homology to transposable elements suggests that the mechanism of silencing involves direct interaction of the piRNA with either the genomic site of the transposable elements or with the retrotransposon transcripts themselves. Interestingly, some transposable elements are embedded in the introns of actively transcribed genes, e.g., Ago3, and in these cases the host gene escapes silencing.  This suggests that the sequence-homology based targeting of piRNAs is cytoplasmic and at the post-transcriptional level.  To test this hypothesis, I am going to compare the silencing of transgenes engineered to contain a piRNA-homologous site within either an exon or an intron.  If only exonic piRNA-homologous sequences show silencing, this would support the hypothesis that the silencing is mediated post-transcriptionally in the cytoplasm.

fan.zhang@umassmed.edu

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