High impact information on spn-E

• Enhanced frequency of TART, but not HeT-A, attachments in individuals carrying one dose of mutant spn-E or aub alleles suggests that TART is a primary target of the RNAi machinery [1].
• At the same time, we detected enhanced HeT-A attachments to broken chromosome ends in oocytes from homozygous spn-E mutants [1].
• These mutations cause an increase in the frequency of telomeric element retrotransposition to a broken chromosome end. spn-E mutations eliminate HeT-A and TART short RNAs in ovaries, suggesting an RNAi-based mechanism in the control of telomere maintenance in the Drosophila germline [1].
• The homeless (hls) gene of Drosophila is required for anteroposterior and dorsoventral axis formation during oogenesis [2].
• As orb, yps and spn-E encode RNA-binding proteins, they may regulate the translation of unidentified RNAs necessary for the polarisation of the microtubule cytoskeleton [3].

Biological context of spn-E

• Analyses of new alleles of spn-E and orb show that both SPN-E and ORB proteins are required to organise the microtubule cytoskeleton at stage 9, and to prevent premature cytoplasmic streaming [3].
• The abundance of telomeric retroelement transcripts is up-regulated owing to mutations in the spn-E and aub genes, encoding a putative RNA helicase and protein of the Argonaute family, respectively, which are related to the RNA interference (RNAi) machinery [1].
• Genes predicted to encode proteins that interact with RNA (egalitarian and orb) are required for the normal subcellular distribution of Bic-D::GFP in the germarium, and another potential RNA binding protein, spn-E, is required for proper transport of Bic-D::GFP from the nurse cells to the oocyte in later oogenesis stages [4].
• Mutation in the spindle-E gene relieving Stellate silencing also leads to a derepression of the other genomic tandem repeats and retrotransposons in the germline [5].

Anatomical context of spn-E

• VASA and AUBERGINE proteins are known as components of perinuclear ribonucleoprotein particles in germ cells, and spn-E mutation disturbs protein content of the particles [6].
• We conclude that hls functions along with Su(Ste) and other recently described genes to repress the Stellate locus in spermatocytes, and that it may also play a role in repressing certain other repeated sequences [7].
• To determine whether the regulatory role of hls is specific for Stellate or includes other repeated sequences as well, we compared testis RNA levels for nine transposable elements and found that all but one, copia, were expressed at the same levels in hls mutants and wild type [7].

Analytical, diagnostic and therapeutic context of spn-E

• Sequence analysis of the hls cDNA predicts a protein with amino-terminal homology to members of the DE-H family of RNA-dependent ATPases and putative helicases [2].

References