Abstract
BackgroundDrosophila retinal architecture is laid down between 24–48 hours after puparium formation, when some of the still uncommitted interommatidial cells (IOCs) are recruited to become secondary and tertiary pigment cells while the remaining ones undergo apoptosis. This choice between survival and death requires the product of the roughest (rst) gene, an immunoglobulin superfamily transmembrane glycoprotein involved in a wide range of developmental processes. Both temporal misexpression of Rst and truncation of the protein intracytoplasmic domain, lead to severe defects in which IOCs either remain mostly undifferentiated and die late and erratically or, instead, differentiate into extra pigment cells. Intriguingly, mutants not expressing wild type protein often have normal or very mild rough eyes.Methodology/Principal FindingsBy using quantitative real time PCR to examine rst transcriptional dynamics in the pupal retina, both in wild type and mutant alleles we showed that tightly regulated temporal changes in rst transcriptional rate underlie its proper function during the final steps of eye patterning. Furthermore we demonstrated that the unexpected wild type eye phenotype of mutants with low or no rst expression correlates with an upregulation in the mRNA levels of the rst paralogue kin-of-irre (kirre), which seems able to substitute for rst function in this process, similarly to their role in myoblast fusion. This compensatory upregulation of kirre mRNA levels could be directly induced in wild type pupa upon RNAi-mediated silencing of rst, indicating that expression of both genes is also coordinately regulated in physiological conditions.Conclusions/SignificanceThese findings suggest a general mechanism by which rst and kirre expression could be fine tuned to optimize their redundant roles during development and provide a clearer picture of how the specification of survival and apoptotic fates by differential cell adhesion during the final steps of retinal morphogenesis in insects are controlled at the transcriptional level.
Highlights
Differential adhesion plays a central role in morphogenesis, allowing cells to sort themselves out from initially unpatterned populations as they become committed to specific fates [1,2], and helping a wide range of cell types, such as neurons, lymphocytes and neural crest cells to navigate and find their interacting partners with exquisite precision [3,4]
Rst protein redistribution in interommatidial cells (IOCs) correlates with changes in rst mRNA levels rstD flies differ from other previously described rst mutant alleles by having ‘‘glassy’’- looking compound eyes with a brownish-red color (Fig. 1A) instead of the usual bright red, rough-like phenotype, by being capable of spontaneously and stably revert both to wild type-like and severe rough eye phenotypes at a moderate frequency (Octacilio-Silva S, Machado M and Ramos RGP, unpublished observations) and by displaying a delay in IOCs intracellular redistribution of Rst protein, which happens 8–10% later in development compared to wild type (Fig. 1B)
Rst mRNA was initially detected at relatively low levels from 0 to 10% development after puparium formation (AFP)
Summary
Differential adhesion plays a central role in morphogenesis, allowing cells to sort themselves out from initially unpatterned populations as they become committed to specific fates [1,2], and helping a wide range of cell types, such as neurons, lymphocytes and neural crest cells to navigate and find their interacting partners with exquisite precision [3,4]. Drosophila retinal architecture is laid down between 24–48 hours after puparium formation, when some of the still uncommitted interommatidial cells (IOCs) are recruited to become secondary and tertiary pigment cells while the remaining ones undergo apoptosis This choice between survival and death requires the product of the roughest (rst) gene, an immunoglobulin superfamily transmembrane glycoprotein involved in a wide range of developmental processes. Both temporal misexpression of Rst and truncation of the protein intracytoplasmic domain, lead to severe defects in which IOCs either remain mostly undifferentiated and die late and erratically or, instead, differentiate into extra pigment cells. Mutants not expressing wild type protein often have normal or very mild rough eyes
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