The Chromosomal Proteins JIL-1 and Z4/Putzig Regulate the Telomeric Chromatin in Drosophila melanogaster
Drosophila telomere maintenance depends on the transposition of the specialized retrotransposons HeT-A, TART, and TAHRE. Controlling the activation and silencing of these elements is crucial for a precise telomere function without compromising genomic integrity. Here we describe two chromosomal proteins, JIL-1 and Z4 (also known as Putzig), which are necessary for establishing a fine-tuned regulation of the transcription of the major component of Drosophila telomeres, the HeT-A retrotransposon, thus guaranteeing genome stability. We found that mutant alleles of JIL-1 have decreased HeT-A transcription, putting forward this kinase as the first positive regulator of telomere transcription in Drosophila described to date. We describe how the decrease in HeT-A transcription in JIL-1 alleles correlates with an increase in silencing chromatin marks such as H3K9me3 and HP1a at the HeT-A promoter. Moreover, we have detected that Z4 mutant alleles show moderate telomere instability, suggesting an important role of the JIL-1-Z4 complex in establishing and maintaining an appropriate chromatin environment at Drosophila telomeres. Interestingly, we have detected a biochemical interaction between Z4 and the HeT-A Gag protein, which could explain how the Z4-JIL-1 complex is targeted to the telomeres. Accordingly, we demonstrate that a phenotype of telomere instability similar to that observed for Z4 mutant alleles is found when the gene that encodes the HeT-A Gag protein is knocked down. We propose a model to explain the observed transcriptional and stability changes in relation to other heterochromatin components characteristic of Drosophila telomeres, such as HP1a. © 2012 Silva-Sousa et al.
Main Authors: | Silva-Sousa, Rute, Lopez-Panades, Elisenda, Piñeyro, David, Casacuberta, Elena |
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Other Authors: | Ministerio de Ciencia e Innovación (España) |
Format: | artículo biblioteca |
Published: |
Public Library of Science
2012-12-13
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Online Access: | http://hdl.handle.net/10261/115906 http://dx.doi.org/10.13039/501100004837 http://dx.doi.org/10.13039/501100001871 |
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