The insect midgut is an important site of entry for pathogens and insect control agents. This review focuses on recent information related to midgut epithelial growth, metamorphosis, and repair as a defense against pathogens. The roles of stem cell mitogens and differentiation factors are described. Included is a discussion of apoptosis and autophagy in the yellow body. Sloughing, also described, protects the midgut from virus infections and bacterial toxins through death and replacement of affected cells. The mechanisms by which the repair process reduces the effectiveness of pest control strategies are discussed. Primary tissue culture methods also are described, and their value in understanding the mechanisms by which biologically based insecticides work is discussed.

Four different human tissues and breast cancer cell lines were screened to identify exon deletion variant transcripts of estrogen receptor L L (ERL L) by reverse transcription-polymerase chain reaction using the 'splice targeted primer approach' that amplifies each category of exon deleted variants as a separate gene population. A total of 10 different variant mRNAs that have deletions in various combination of exons were identified by sequence analysis. They were exon 2v v; exons 2 and 5^6v v; exon 3v v; exon 4v v; exon 5v v; exons 5 and 2v v; exon 6v v; exons 6 and 2v v; exons 6, 2^3v v; and exons 5^6v v. In some cases, deletion of an exon appears to be associated with a mutation of a specific base. Although ERK K and ERL L are highly homologous, have identical exon and functional domain organization, exhibit similar ligandbinding profiles and interact with identical DNA response elements, the sequence of exon skipping in ERL L pre-mRNA appears to be distinct from that of ERK K mRNA. Furthermore, results described here also suggest that alternate splicing of ERL L mRNA is tissue specific. The presence of a ERL L variant profile together with other ER isoforms in a tissue may have functional implications in binding and response to a particular ligand. ß

We describe here the cloning and functional characterization of two unique ER isoforms, ERbeta4 and ERbeta5. The full length ERbeta4 and ERbeta5 were identified by asymmetric PCR using human ovary cDNA, cloning, and sequence analyses. Both receptors share identical sequences with ERbeta1 from exon 1 to exon 7. In the place of exon 8, ERbeta4 has unique sequences arising from a region downstream of the ERbeta gene and upstream of the SYNE2 gene. ERbeta5 has sequences arising from retention of the 5' end of the intron between exon 7 and 8. Both receptors bind promoter sequences on DNA but do not bind estrogen. They translocate to the nucleus and exhibit three to four times higher estrogen-independent transcriptional activity than ERbeta1. When co-transfected with ERalpha, they predominantly form heterodimers and negatively regulate its transcriptional activity. Estrogen-independent transcriptional activity of ERbeta5, but not ERbeta4, was inhibited by ERalpha, demonstrating for the first time that ERalpha regulates ERbeta. Tissue-specific expression of ERbeta4 and ERbeta5, together with their ligand-independent transcriptional properties and ERalpha modulating activities, could have a number of implications in seemingly unlinked biological processes regulated by estrogen.

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