Mechanosensory transduction by vertebrate hair cells depends on a protein complex at the tips of shorter stereocilia associated with mechanoelectrical transduction channels activated by tip links in the hair bundle. In mammalian hair cells, this complex includes transmembrane channel-like protein subunit 1 (TMC1), lipoma HMGIC fusion partner-like 5 protein (LHFPL5) and protocadherin 15 (PCDH15), a lower-end component of the tip link. TMC1 interacts with LHFPL5 and PCDH15 but how the complex develops to maturity, and the relationships between these proteins, remains uncertain. Here we evaluate the spatiotemporal development of LHFPL5 distributions in mouse cochlear hair bundles by immunofluorescence and immunogold transmission electron microscopy, from postnatal day 0 (P0) through P21 in wild type and PCDH15-deficient mice. At P0, hair bundles contain many short microvilli-like processes which we term unranked stereocilia, and a subset of lengthening rows, adjacent to a kinocilium. LHFPL5 is distributed throughout the bundle, including on stereocilia tips and the kinocilium. At P3, 4-to-6 rows of ranked stereocilia are evident, total LHFPL5 expression peaks, and LHFPL5 is localised to ranked stereocilia tips of all rows and to lower shaft/ankle links. By P12, the bundle has a mature pattern with 3 ranked rows but virtually no unranked stereocilia or kinocilium; LHFPL5 expression has declined and become restricted to the tips of shorter stereocilia. Throughout development from P0, expression of LHFPL5 is greater overall on apical than basal bundles, but there is, on average, an equal amount of labelling per labelled tip. In P3 mice lacking PCDH15, LHFPL5 labelling is not at the tips but is primarily on unranked stereocilia and lower lateral links. These data show that LHFPL5 is already present in the MET apparatus at P0 but requires PCDH15 at P3 to remain there. Shaft/ankle link localisation suggests it interacts with link proteins other than PCDH15.

In task switching, extending the response-cue interval (RCI) reduces the switch cost-the detriment to performance when switching compared to repeating tasks. This reduction has been used as evidence for the existence of task-set decay processes. Recently, this has been challenged by the observation of sequential dependencies on the RCI effect: switch cost is only reduced at longer RCIs when the previous trial had a short RCI. This trialwise variation of RCI is thought to affect the temporal distinctiveness (TD) of a previous task's episodic trace, affecting the probability of its automatic retrieval on the current trial; importantly, TD is thought to be independent of the current trial's RCI. The present study highlights a dependency between the current RCI and TD, and demonstrates that a decay model can reproduce some patterns of data attributed to TD. Further, the decay account makes a strong prediction when TD is held constant: repetition response times should slow as RCI increases, and switch response times should be facilitated. This prediction was tested via re-analysis of extant data and three experiments. The re-analysis provided some evidence for the decay account, but Experiments 1 and 2 report slowing for task repetition and switch trials, which cannot be explained by a task-set decay process. Experiment 3, which utilised tasks requiring perceptual judgements, showed small evidence for decay. We conclude that the data are largely consistent with the TD account and that the evidence for decay of higher-level task-sets is not convincing.

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