Abstract
The imaginal discs of the genetically tractable model organism Drosophila melanogaster have been used to study cell-fate specification and plasticity, including homeotic changes and regeneration-induced transdetermination. The identity of the reprogramming mechanisms that induce plasticity has been of great interest in the field. Here we identify a change from antennal fate to eye fate induced by a Distal-less-GAL4 (DllGAL4) P-element insertion that is a mutant allele of Dll and expresses GAL4 in the antennal imaginal disc. While this fate change is not induced by tissue damage, it appears to be a hybrid of transdetermination and homeosis as the GAL4 expression causes upregulation of Wingless, and the Dll mutation is required for the fate change. Neither GAL4 expression nor a Dll mutation on its own is able to induce antenna-to-eye fate changes. This plasticity appears to be unique to the DllGAL4 line, possibly due to cellular stress induced by the high GAL4 expression combined with the severity of the Dll mutation. Thus, we propose that even in the absence of tissue damage, other forms of cellular stress caused by high GAL4 expression can induce determined cell fates to change, and selector gene mutations can sensitize the tissue to these transformations.
Highlights
Normal development requires that cells become progressively restricted in their potential as they become determined and differentiate toward specific fates
DllGAL4 animals that were maintained at 18 °C rarely showed antennal defects, while animals maintained at 25 °C or shifted to 30 °C during early third instar for 24 hours showed a high frequency of defects, including altered morphology in the arista and the third antennal segment (Fig. 1b–b””)
While it remains possible that an enhancer is present that is tightly linked to the DllGAL4, we propose that some unique combination of the strength of GAL4 expression and severity of the Dll mutation in the DllGAL4 line enable this unprecedented plasticity in the antennal disc
Summary
Normal development requires that cells become progressively restricted in their potential as they become determined and differentiate toward specific fates This determination of fate is regulated by homeotic or selector genes[1]. Homeosis occurs when mutations are generated in hox or selector genes, which are important for establishing cell, tissue and segment identities. These mutations result in replacement of one body part by another[5]. Misexpression of selector genes can result in transformations that phenotypically resemble transdetermination[5,19] It remains to be seen whether cell fate plasticity can be induced through mechanisms other than tissue damage, such as general cellular stress, mechanical tension, or activation of alternative signaling pathways
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