A set of ER-localized membrane proteins whose loss causes developmental diseases in humans, assemble with Sec61 into a translocon that facilitates the biogenesis of hundreds of different multi-pass membrane proteins.
By linking export and licensing of a piRNA precursor transcript, channel nuclear pore complex subunits Nup54 and Nup58 are specifically required to silence transposons in the Drosophila ovary.
Heterochromatin formation at transposon loci depends on dimerisation of the effector complex that elicits co-transcriptional silencing and this requirement is fulfilled by co-option of the conserved dimerisation hub protein, Cut-up/LC8.
Structural and biochemical analyses of a eukaryotic DNA transpososome in the integration step reveal how mariner/Tc1 transposons are selectively integrated into a TA target sequence.
Maternally deposited Piwi-piRNA complexes co-transcriptionally repress transposable elements that transiently become active in somatic cells of the developing Drosophila embryo.
A DNA transposon, or ‘jumping gene’, controls its amplification within a genome through a competition between the enzyme multimers that are responsible for its mobility.
Transposon activation during male gametogenesis is caused by interactions between DNA demethylation and linker histone H1, developmental depletion of which promotes pollen fertility.
A member of the Drosophila Nuclear Export Factor (Nxf) family, Nxf2, forms part of the piRNA-dependent co-transcriptional silencing complex and is essential for transposon repression in fly ovaries.
Genetic, structural, and biochemical analyses of IS607-family transposons shows that the DNA translocation reaction proceeds very differently from other reactions promoted by serine recombinases.
