, Volume 86, Issue 3, pp 203-215

Drosophila simulans Lethal hybrid rescue mutation (Lhr) rescues inviable hybrids by restoring X chromosomal dosage compensation and causes fluctuating asymmetry of development

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Abstract

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.