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Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis.

ABSTRACT: The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, suggesting that there are additional targets. To identify uncharacterized transcriptional targets of Trh and to further understand the role of Trh in embryonic tracheal formation, we performed an in situ hybridization screen using a library of ~100 tracheal-expressed genes identified by the Berkeley Drosophila Genome Project (BDGP). Surprisingly, expression of every tracheal gene we tested was dependent on Trh, suggesting a major role for Trh in activation and maintenance of tracheal gene expression. A re-examination of the interdependence of the known early-expressed transcription factors, including trh, ventral veinless (vvl) and knirps/knirps-related (kni/knrl), suggests a new model for how gene expression is controlled in the trachea, with trh regulating expression of vvl and kni, but not vice versa. A pilot screen for the targets of Vvl and Kni/Knrl revealed that Vvl and Kni have only minor roles compared to Trh. Finally, genome-wide microarray experiments identified additional Trh targets and revealed that a variety of biological processes are affected by the loss of trh.

SUBMITTER: Chung S

PROVIDER: S-EPMC3215829 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature

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Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis.

Chung SeYeon S Chavez Cy C Andrew Deborah J DJ

Developmental biology 20110922 1

The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, sugges ...[more]

PMID: 21963537

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Project description:Abstract: The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, suggesting that there are additional targets. To identify uncharacterized transcriptional targets of Trh and to further understand the role of Trh in embryonic tracheal formation, we performed an in situ hybridization screen using a library of ~100 tracheal-expressed genes identified by the Berkeley Drosophila Genome Project (BDGP). Surprisingly, expression of every tracheal gene we tested was dependent on Trh, suggesting a major role for Trh in activation and maintenance of tracheal gene expression. A re-examination of the interdependence of the known early-expressed transcription factors, including trh, ventral veinless (vvl) and knirps/knirps-related (kni/knrl), suggests a new model for how gene expression is controlled in the trachea, with trh regulating expression of vvl and kni, but not vice versa. A pilot screen for the targets of Vvl and Kni/Knrl revealed that Vvl and Kni have only minor roles compared to Trh. Finally, genome-wide microarray experiments identified additional Trh targets and revealed that a of biological processes are affected by the loss of trh. Goals: The goals of the microarray experiments were to identify additional targets of the Trh transcription factor to learn the range of genes regulated by this transcription factor during embryogenesis. Our in situ screen revealed that Trh is required for all tested tracheal genes. Our new data now shows that Trh affects a range of biological processes. RNA was isolated from stage 11-16 wild type Drosophila embryos and compared to RNA from trh null mutant embryos of the same age; all samples were hybridized to the Drosophila Genome 2.0 Affymetrix array. Three individual replicates were obtained for each sample.

Project description:BackgroundIn Drosophila embryos, checkpoints maintain genome stability by delaying cell cycle progression that allows time for damage repair or to complete DNA synthesis. Drosophila MOF, a member of MYST histone acetyl transferase is an essential component of male X hyperactivation process. Until recently its involvement in G2/M cell cycle arrest and defects in ionizing radiation induced DNA damage pathways was not well established.ResultsDrosophila MOF is highly expressed during early embryogenesis. In the present study we show that haplo-insufficiency of maternal MOF leads to spontaneous mitotic defects like mitotic asynchrony, mitotic catastrophe and chromatid bridges in the syncytial embryos. Such abnormal nuclei are eliminated and digested in the yolk tissues by nuclear fall out mechanism. MOF negatively regulates Drosophila checkpoint kinase 2 tumor suppressor homologue. In response to DNA damage the checkpoint gene Chk2 (Drosophila mnk) is activated in the mof mutants, there by causing centrosomal inactivation suggesting its role in response to genotoxic stress. A drastic decrease in the fall out nuclei in the syncytial embryos derived from mof¹/+; mnkp⁶/+ females further confirms the role of DNA damage response gene Chk2 to ensure the removal of abnormal nuclei from the embryonic precursor pool and maintain genome stability. The fact that mof mutants undergo DNA damage has been further elucidated by the increased number of single and double stranded DNA breaks.Conclusionmof mutants exhibited genomic instability as evidenced by the occurance of frequent mitotic bridges in anaphase, asynchronous nuclear divisions, disruption of cytoskeleton, inactivation of centrosomes finally leading to DNA damage. Our findings are consistent to what has been reported earlier in mammals that; reduced levels of MOF resulted in increased genomic instability while total loss resulted in lethality. The study can be further extended using Drosophila as model system and carry out the interaction of MOF with the known components of the DNA damage pathway.

Dataset Information

Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis.

Publications

Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis.

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