title: The chromosomal proteins JIL-1 and Z4/Putzig regulate the telomeric chromatin in Drosophila melanogaster.
abstract: 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.
authors.affiliation: Institute of Evolutionary Biology, Institut de Biologia Evolutiva (CSIC-UPF), Barcelona, Spain.
authors.forename: Rute
authors.initials: R
authors.lastname: Silva-Sousa
authors.forename: Elisenda
authors.initials: E
authors.lastname: López-Panadès
authors.forename: David
authors.initials: D
authors.lastname: Piñeyro
authors.forename: Elena
authors.initials: E
authors.lastname: Casacuberta
mesh_terms: D000818:Animals; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D002843:Chromatin / Q000235:genetics / Q000378:metabolism; D000090266:Chromobox Protein Homolog 5; D002868:Chromosomal Proteins, Non-Histone / Q000378:metabolism; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster; D015683:Gene Products, gag / Q000235:genetics / Q000378:metabolism; D042822:Genomic Instability; D011495:Histone-Lysine N-Methyltransferase / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D018626:Retroelements / Q000235:genetics; D016615:Telomere / Q000235:genetics / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D002843:Chromatin; D002868:Chromosomal Proteins, Non-Histone; D029721:Drosophila Proteins; D015683:Gene Products, gag; C103996:HeT-A-gag protein, Drosophila; D018626:Retroelements; C469435:TART-element-gag protein, Drosophila; C524392:pzg protein, Drosophila; D000090266:Chromobox Protein Homolog 5; D011495:Histone-Lysine N-Methyltransferase; C507306:JIL-1 protein, Drosophila; D017346:Protein Serine-Threonine Kinases