Exploring insect biodiversity: the parasitic Hymenoptera, chiefly Chalcidoidea, associated with seeds of asphodels (Xanthorrhoeaceae), with the description of nine new species belonging to Eurytomidae and Torymidae.

An account is given of the communities of Chalcidoidea, mostly based upon species of Bruchophagus Ashmead (Eurytomidae), which feed as larvae in seeds of Asphodelus and Asphodeline (Xanthorrhoeaceae). Eight new species of Eurytomidae, namely B. abscedus Askew sp. n., B. asphodelinae Askew Stojanova sp. n., B. gijswijti Askew Ribes sp. n., B. insulare Delvare sp. n., B. lecomtei Delvare sp. n., B. ribesi Askew sp. n., Eurytoma genale Askew Stojanova sp. n., and Aximopsis balajasi Delvare sp. n., are described together with the new species Idiomacromerus asphodeli Ribes sp. n. (Torymidae). Eurytoma setigera Mayr, 1878 is again synonymized with E. pistaciae Rondani, 1877 syn. rev. Puklina dillerae Doganlar, 1993 and P. asphodelinae Boyadzhiev, 2003 are synonymized with P. depilata Graham, 1987 syn n. The use, respectively of the mitochondrial genes COI and Cyt B and of the nuclear gene EF1-α, allowed us to discriminate pairs of sibling species in the three genera of Eurytomidae and to circumscribe the limits of the hypervariable Eurytoma asphodeli Hedqvist, 1976. The trophic webs associated with five species/subspecies of asphodels are fully described and illustrated, the distributions of the chalcid wasps involved are figured, and the phenology of the most common species is quoted and figured.

New model systems provide insights into Myc-induced transformation.

The ability of Myc to promote cellular transformation is well established; however, a better understanding of the mechanisms through which Myc mediates tumorigenesis is essential for the development of therapeutic approaches to target this potent oncoprotein. Structure-function studies in rodent fibroblast cells have provided the basis for much of our current understanding of these mechanisms. To build on these approaches, we have characterized three novel human cell line models of Myc-dependent transformation: MCF10A, SH-EP Tet21/N-Myc, and LF1/TERT/LT/ST cells. We have also evaluated Myc family proteins (c-Myc and L-Myc), a naturally occurring isoform of Myc (MycS), and a set of N-terminal domain mutants (ΔMBII, W135E, T58A) for their ability to promote anchorage-independent growth in these models. Taken together, these results provide the field with three new human cell-based models to study Myc activity, highlight the importance of cellular context, and challenge the paradigm that the ability of Myc to promote tumorigenesis is exclusively MBII-dependent.

Repression of the human immunodeficiency virus type-1 long terminal repeat by the c-Myc oncoprotein.

The effect of trans-acting factors on cis-acting DNA elements on the HIV-1 promoter are the principal determinant regulating transcriptional activation and repression. Host factors that limit viral replication can contribute to the emergence and maintenance of proviral reservoirs. The current paradigm is that this sub-population of latently infected cells confers a biological advantage to the virus by facilitating evasion of immunologic responses and therapeutic strategies resulting in life-long and persistent infection. In this report, we show that ectopic expression of the nuclear phosphoprotein, c-Myc can inhibit HIV-1 gene expression and virus production in CD4+ T-lymphocytes. The effect exerted does not appear to involve other known functions of c-Myc such as proliferation, or apoptosis. The mechanism does implicate c-Myc in a direct role. We have found evidence that c-Myc can specifically recognize the HIV-1 initiator element surrounding the start site of transcription and linker scanning mutagenesis experiments confirmed a loss of c-Myc-mediated repression in the absence of this region. Moreover, we show that c-Myc can interact with the initiator binding proteins YY-1 and LBP-1 and can cooperate with these factors to synergistically repress HIV-1 LTR transcription. Taken together, these results indicate that c-Myc is an important regulator of HIV-1 transcription that potentially contributes to the latent proviral state.