Drosophila melanogaster males lack recombination and have evolved a mechanism of meiotic chromosome segregation that is independent of both the chiasmatic and achiasmatic segregation systems of females. The teflon (tef ) gene is specifically required in males for proper segregation of autosomes and provides a genetic tool for understanding recombination-independent mechanisms of pairing and segregation as well as differences in sex chromosome vs. autosome segregation. Here we report on the cloning of the tef gene and the molecular characterization of tef mutations. Rescue experiments using a GAL4-driven pUAS transgene demonstrate that tef corresponds to predicted Berkeley Drosophila Genome Project (BDGP) gene CG8961 and that tef expression is required in the male germ line prior to spermatocyte stage S4. Consistent with this early prophase requirement, expression of tef was found to be independent of regulators of meiotic M phase initiation or progression. The predicted Tef protein contains three C2H2 zinc-finger motifs, one at the amino terminus and two in tandem at the carboxyl terminus. In addition to the zinc-finger motifs, a 44-to 45-bp repeat is conserved in three related Drosophila species. On the basis of these findings, we propose a role for Tef as a bridging molecule that holds autosome bivalents together via heterochromatic connections.

Sarcomas are rare tumors with devastating clinical consequences, often affecting children as well as adults. Brain metastasis in sarcoma is frequently preceded by lung metastasis. Common offenders include Ewing sarcoma, osteosarcoma and leiomyosarcoma. Although our understanding of sarcoma metastasis remains limited, several cellular factors and signaling pathways appear to play regulatory roles and/or exhibit prognostic values in sarcoma metastasis. In addition, MicroRNAs have been shown to have either positive or negative impact on sarcoma biology and metastasis. Sarcoma is considered one of the classic radio- and chemo-resistant brain metastasis, hence the use of multiple modalities in order to improve the therapeutic ratio and overcome the inherent resistance. Treatment modalities include surgical resection, chemotherapy, gamma knife radiosurgery and/or fractionated whole-brain radiotherapy. The efficacy of chemotherapy is limited by the ability of the drug(s) to cross the blood-brain barrier (BBB), and the chemosensitivity of the tumor to the chemotherapeutic agent. In this review, we discuss the pathology, biology and therapy for sarcoma brain metastasis.

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