Maintenance of an intact genome and proper regulation of the genes within are crucial aspects for life. The work of this dissertation has implicated the Drosophila condensin II complex in both processes. Condensin II's ability to reconfigure chromosomes into spatially separated and discrete units is necessary to ensure proper meiotic segregation. When this "individualization" activity fails in a condensin II mutant, chromosomes remain entangled, and either cosegregate or become lost during cell division. This leads to the creation of aneuploid sperm. We have also implicated condensin II as a factor necessary to individualize interphase somatic chromosomes from one another. This is relevant in Drosophila because the association of homologous chromosomes is thought to facilitate gene regulation activity in trans. We speculate that condensin II individualization spatially distances aligned chromosomes from one another and prevents this trans-communication between allelic loci. This is supported first by an increase of homologous chromosome pairing in a condensin II mutant background. Secondly, loss of condensin II leads to elevated production from alleles that are known to depend on pairing for transcriptional activation. These meiotic and interphase condensin II roles support its necessity to Drosophila genome integrity and transcriptional regulation. Given the conservation of condensin from bacteria to humans, it is likely that equivalent or related roles exist in a variety of species.

Drosophila male is an example of achiasmatic meiosis which lacks crossingover and chiasmata during meiosis. Previous studies showed that homologous pairing of both euchromatin and centromeres is lost during middle prophase I, however, homologs are still connected as they form bivalents. The X-Y pair utilizes a specific repeated sequence within the heterochromatic ribosomal DNA blocks as a pairing site. No pairing sites have yet been identified for the autosomes. To search for such sites, we utilized probes specifically targeting heterochromatin regions to assay pairing sequences and behavior in meiosis by fluorescence in situ hybridization (FISH). We found that the fourth homologs pair at the heterochromatic region 61 and associate with the X chromosome throughout prophase I. The pairing of the fourth homologs is disrupted in the homolog conjunction complex mutants. Conversely, six tested heterochromatic regions of the major autosomes (second and third chromosomes) have proved to be largely unpaired after early prophase I. This suggests that pairing mechanism of the major autosomes may differ from the sex and fourth chromosomes; stable connections between major autosomal homologs might occur at different sites along chromosomes in different cells by analogy to chiasmata. Moreover, FISH analysis also revealed two distinct patterns of sister chromatid cohesion in heterochromatin: regions with stable cohesion and regions lacking cohesion, suggesting that sister chromatid cohesion is incomplete within heterochromatin but with preferential sites in male meiosis.Modifier of Mdg4 in Meiosis (MNM) and Stromalin in Meiosis (SNM) are components of homolog conjunction complex and essential for homolog pairing and segregation in male meiosis. Using yeast two-hybrid assay and co-immunoprecipitation, we showed that the MNM and SNM interact with each other. Specifically, the BTB domain of MNM is responsible for the interaction with SNM, whereas FLYWCH domain of MNM is crucial for this interaction but does not directly interact with SNM. Additionally, point mutation analysis revealed that L9K replacement of the BTB domain weakened the MNM-SNM interaction and caused high frequencies of chromosome nondisjunction. In conclusion, these results provide a biochemical basis for the mechanism of homolog pairing and support the role of homolog conjunction complex in male meiosis.