The Drosophila βFTZ-F1 Orphan Nuclear Receptor Provides Competence for Stage-Specific Responses to the Steroid Hormone Ecdysone

Abstract

The acquisition of competence is a key mechanism for refining global signals to distinct spatial and temporal responses. The molecular basis of competence, however, remains poorly understood. Here, we show that the beta FTZ-F1 orphan nuclear receptor functions as a competence factor for stage-specific responses to the steroid hormone ecdysone during Drosophila metamorphosis. beta FTZ-F1 mutants pupariate normally in response to the late larval pulse of ecdysone but display defects in stage-specific responses to the subsequent ecdysone pulse in prepupae. The ecdysone-triggered genetic hierarchy that directs these developmental responses is severely attenuated in beta FTZ-F1 mutants, although ecdysone receptor expression is unaffected. This study define beta FTZ-F1 as an essential competence factor for stage-specific responses to a steroid signal and implicates interplay among nuclear receptors as a mechanism for achieving hormonal competence.

Nuclear receptor BgFTZ‐F1 regulates molting and the timing of ecdysteroid production during nymphal development in the hemimetabolous insect Blattella germanica

“…FTZ-F1 has been defined as a transcriptional competence factor of 20E action in dipterans. In ␤FTZ-F1 mutants of D. melanogaster, the expression of the 20E-dependent genes Br-C, E74A, E75A, and E93 is clearly attenuated during the prepupal-pupal transition (Broadus et al, 1999). Furthermore, ␤FTZ-F1 plays the role of competence factor in adult fat bodies during the previtellogenic-vitellogenic transition of A. aegypti.…”

“…Furthermore, the presence of ␤FTZ-F1 during the prepupal stage plays a crucial role as a competence factor for stage-specific responses to a second 20E pulse that triggers the onset of pupal development. Thus, ␤Ftz-F1 mutants show defects in adult head eversion, leg elongation and salivary gland degeneration at the prepupal-pupal transition (Broadus et al, 1999). The role of FTZ-F1 in molting has also been demonstrated in the coleopteran Tribolium castaneum (Tan and Palli, 2008), whereas its role as a competence factor for 20E action has been reported during the previtellogenic-vitellogenic transition in the dipteran Aedes aegypti (Li et al, 2000;Zhu et al, 2003).…”

Autophagic programmed cell death in Drosophila

“…[45][46][47][48][49][50] The ecdysone receptor complex, and the nuclear receptor competence factor bFTZ-F1, activate transcription of the early genes BR-C, E74A, and E93. 51,52 Salivary glands are not destroyed in animals with mutations in bFTZ-F1, BR-C, E74A, and E93. [52][53][54][55] While bFTZ-F1 and E93 mutants exhibit defects in vacuolar changes during salivary gland autophagic cell death, BR-C and E74A mutant salivary glands progress to a very late stage in cell death even though complete destruction is prevented.…”

Fhos encodes a Drosophila Formin‐Like Protein participating in autophagic programmed cell death

“…3B) exhibit persistent LSGs. This phenotype could be considered a ''hallmark'' phenotype of several mutations affecting steroid-regulated genes such as BR-C and E93 (Baehrecke and Broadus et al, 1999;Fletcher and Thummel, 1995;Lee and Baehrecke, 2001). …”

“…Also, in response to the second hormonal pulse, the transcription of the stage-specific gene E93 is induced. Although all these genes are necessary for the salivary gland PCD to take place, the E93 gene seems to play a more specific role by modulating cytoplasmic dynamic changes during salivary gland cell death since mutations in E93 do not exhibit normal changes in vacuole size and membrane breakdown (Lee and Baehrecke, 2001), while BR-C and E74A are pleiotropic (Broadus et al, 1999;Jiang et al, 2000;Lee and Baehrecke, 2000;Lee et al, , 2002Martin and Baehrecke, 2004;Restifo and White, 1992).…”