Abstract: Disclosed is a Drosophila grim gene and encoded GRIM polypeptide, an activator of apoptosis. The disclosed nucleic acid sequences are useful in the production of the protein and as hybridization probes and primers. Expression of the GRIM protein causes programmed cell death. Preferred embodiments include expression of grim under the control of an inducible promoter and the use of such a construct in the control of an insect population.

Abstract: Disclosed is a Drosophila grim gene and encoded GRIM polypeptide, an activator of apoptosis. The disclosed nucleic acid sequences are useful in the production of the protein and as hybridization probes and primers. Expression of the GRIM protein causes programmed cell death. Preferred embodiments include expression of grim under the control of an inducible promoter and the use of such a construct in the control of an insect population.

Abstract: The present invention relates to cell death genes, which are genes required for programmed cell deaths; mutant organisms, in which embryonic programmed cell death occurs to a less than normal extent; proteins encoded by the cell death genes; antibodies which bind the cell death gene products; and agents which alter the ability of cell death genes to cause programmed death of cells. As described herein, Applicants have identified two genes which function in the initiation of apoptosis or programmed cell death. These two genes, referred to respectively as the reaper (rpr) gene and the head involution defective (hid) gene, map to position 75C1,2 on the third chromosome in Drosophila (D.) melanogaster and, as described in detail below, exhibit expression patterns related to the pattern of cell death during Drosophila embryogenesis; mutations in each gene reduce levels of cell deaths or abolish cell death.

Abstract: DNA constructs are provided employing intronically positioned expression, systems, where one of the genes is a dominant gene, usually amplifiable, and the other gene encodes a sequence of interest. Higher levels of co-expression are achieved than when the genese are ligated in tandem. Specifically, the gene of interest is inserted into the intron of a DHFR minigene, the construct transformed into a mammalian cell and the resulting transformants stressed with progressively increasing levels of methotrexate. Substantially increasing levels of co-expression are achieved with increasing levels of methotrexate.