My guess would be transposon suppression rather than evolving away all of the transposons—upregulating existing repression mechanisms would be easier than removing every single active transposon copy. Though I’d still be interested in the test—even if suppression is the main mechanism, I’d still be interested to see how the number of transposons in naked mole rats compare to other rodents. (It is a nontrivial test to run, though—DNA sequencing is particularly unreliable when it comes to transposons, because there are so many near-copies.)
Alternatively, it’s also plausible that the naked mole rat’s defenses are elsewhere in the chain. In particular, they live in a low-oxygen environment, so it’s often speculated that they have very low ROS levels. If that’s the case, we’d still expect transposons to copy occasionally, but cellular-stress-events in which DNA is damaged by ROS, and transposons are temporarily less-repressed while the damage is repaired, would be much more rare.
My guess would be transposon suppression rather than evolving away all of the transposons—upregulating existing repression mechanisms would be easier than removing every single active transposon copy. Though I’d still be interested in the test—even if suppression is the main mechanism, I’d still be interested to see how the number of transposons in naked mole rats compare to other rodents. (It is a nontrivial test to run, though—DNA sequencing is particularly unreliable when it comes to transposons, because there are so many near-copies.)
Alternatively, it’s also plausible that the naked mole rat’s defenses are elsewhere in the chain. In particular, they live in a low-oxygen environment, so it’s often speculated that they have very low ROS levels. If that’s the case, we’d still expect transposons to copy occasionally, but cellular-stress-events in which DNA is damaged by ROS, and transposons are temporarily less-repressed while the damage is repaired, would be much more rare.