THE ORGANIZATION AND EXPRESSION OF THE DROSOPHILA MELANOGASTER HISTONE GENES AND INTERSPERSED MOBILE ELEMENTS (REPEATED, PSEUDOGENES)

The histone genes of Drosophila melanogaster are known to be reiterated and clustered at a single chromosomal locus, 39D-E on the left arm of the second chromosome. In this thesis, the organization of this locus is described. The locus consists of roughly 100 copies of a repeating unit reiterated in tandem. Each repeat unit contains one copy of each of the five histone genes, and genes of opposite transcriptional polarity are interdigitated. The gene order is H3-H4-H2a-H2b-H1, with H3 transcribed right to left and each successive gene of opposite polarity.

There are five primary transcripts from this repeating unit, each corresponding closely to its corresponding mature histone mRNA.

There are two types of repeat unit at 39D-E which differ in length, 4.8 and 5.0 kilobase pairs, and are generally segregated from one another at this locus. This length heterogeneity arises from a substitution in the H3-H1 spacer. The nucleotide sequence of these two types of repeat unit is otherwise remarkably similar.

The tandem arrays of repeat units are occasionally interrupted. These interruptions represent mobile element insertions. Two of these mobile elements are members of different families that appear to transpose via reverse transcription of polyadenylated mRNAs.

The ends of the histone gene tandem arrays have been cloned and characterized. Both ends are composed of large blocks of scrambled repetitive sequences. The DNA sequences just beyond the junctions with histone DNA are composed of short tandemly repeated and inverted repeat sequences.

The histone gene sequences at the ends of the locus indicate that a mechanism other than or in addition to unequal crossing over must operate to maintain sequence homogeneity of the repeat units.

A histone H2b pseudogene has been characterized. It is located in the heterochromatin and consists of only the transcribed portion of the H2b gene, truncated at the 3' end. I propose that this pseudogene arose via reverse transcription of an H2b mRNA self-primed by complementary sequences within the 3' end of the mRNA.