The Drosophila simulans Lhr rescues lethal hybrids from the cross of D. melanogaster and D. simulans. We describe here, the phenotypes of Lhr dependent rescue hybrids and demonstrate the effects of Lhr on functional morphology of the salivary chromosomes in the hybrids. Our results reveal that the phenotypes of the ‘Lhr dependent rescued’ hybrids were largely dependent on the genetic background and the dominance in species and hybrids, and not on Lhr. Cytological examination reveal that while the salivary chromosome of ‘larval lethal’ male carrying melanogaster X chromosome was unusually thin and contracted, in ‘rescued’ hybrid males (C$_{mel}𝑋_{mel}𝑌_{sim}$;A$_{mel}𝐴_{sim}$) the X chromosome showed typical pale staining, enlarged diameter and incorporated higher rate of ³H-uridine in presence of one dose Lhr in the genome. In hybrid males carrying simulans X chromosome (C$_{mel}𝑋_{sim}𝑌_{mel}$;A$_{mel}𝐴_{sim}$), enlarged width of the polytene X chromosome was noted in most of the nuclei, in Lhr background, and transcribed at higher rate than that of the single X chromosome of male. In hybrid females (both viable, e.g., C$_{mel}$ X$_{mel}$ X$_{sim}$; A$_{mel}$ A$_{sim}$ and rescued, e.g., C$_{mel}$ X$_{mel}$ X$_{mel}$; A$_{mel}$ A$_{sim}$), the functional morphology of the X chromosomes were comparable to that of diploid autosomes in presence of one dose of Lhr. In hybrid metafemales, (C$_{mel}𝑋_{mel}𝑋_{mel}𝑋_{sim}$; A$_{mel}𝐴_{sim}$), two dose of melanogaster X chromosomes and one dose of simulans X chromosome were transcribed almost at ‘female’ rate in hybrid genetic background in presence of one dose of Lhr. In rescued hybrid males, the melanogaster-derived X chromosome appeared to complete its replication faster than autosomes. These results together have been interpreted to have suggested that Lhr suppresses the lethality of hybrids by regulating functional activities of the X chromosome(s) for dosage compensation.

In Drosophila melanogaster, the intersex (ix) is a terminally positioned gene in somatic sex determination hierarchy and function with the female specific product of double sex (DSX^F) to implement female sexual differentiation. The null phenotype of ix is to transform diplo-X individuals into intersexes while leaving haplo-X animals unaffected. This study on the effect of different intersex mutations on genital disc development provides the following major results: (i) similar range of a characteristic array of morphological structures (from almost double sex terminalia to extreme reduction of terminal appendages) was displayed by the terminalia of XX ix¹/ix¹, XX ix²/ix² and XX ix⁵/ix⁵ individuals; (ii) an increased number of apoptotic cells were found to occur in a localized manner in mature third instar larval genital discs of ix individuals; (iii) ix mutations can induce high frequency of neoplastic tumours in genitals in the presence of decapentaplegic (dpp^disk) mutations; and (iv) heteroallelic combinations of dpp^disk mutations can also induce tumours in intersex genitals with variable expressivity. On the basis of these findings, we suggest that: (i) loss of function of ix causes massive cell death in both male and female genital primordia of genital discs, resulting phenotype mimicking in male and female characteristics in genitals; and (ii) at the discs, the apoptotic cells persist as ‘undead’ cells that can induce oncogenic transformation in the neighbouring disc cells when dpp signalling is blocked or reduced by dpp^disk mutations.