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Biology subjects

Gough, R.

Publications and source records attributed to Gough, R..

2 recordsLinked to original sources

Extrastriate activity reflects the absence of local retinal input

The physiological blind spot corresponds to the optic disc where the retina contains no light-detecting photoreceptor cells. Our perception seemingly fills in this gap in input. Here we suggest that rather than an active process, such perceptual filling-in could instead be a consequence of the integration of visual inputs at higher stages of processing discounting the local absence of retinal input. Using functional brain imaging, we resolved the retinotopic representation of the physiological blind spot in early human visual cortex and measured responses while participants perceived filling-in. Responses in early visual areas simply reflected the absence of visual input. In contrast, higher extrastriate regions responded more to stimuli in the eye containing the blind spot than the fellow eye. However, this signature was independent of filling-in. We argue that these findings agree with philosophical accounts that posit that the concept of filling-in of absent retinal input is unnecessary.

neuroscience↗

Binding partner regulation of Myosin VI: Loss of tumour-suppressor Dab2 leads to enhanced activity of nuclear myosin

Myosin VI is involved in a variety of cellular processes ranging from endocytosis to transcription. This multi-functional potential is achieved through alternative isoform splicing and through the interaction with a diverse network of binding partners. However, the interplay between the two modes of regulation remains unexplored. To this end, we have compared two different binding partners, Dab2 and CALCOCO2/NDP52, and their interaction with two myosin VI splice isoforms. We found that both isoforms adopt an auto-inhibited state and are subsequently activated by binding partner association. However, differential regulation is achieved through a high and a low affinity binding motifs within myosin VI, with one isoform having the high affinity site blocked. This allows competition between partners and links isoform splicing with binding partner selectivity. Dab2 competition hinders the activity of nuclear myosin VI by preventing DNA binding and transcription. Moreover, re-introduction of Dab2 in the Dab2-deficient MCF-7 cells leads to a decrease in myosin VI-dependent estrogen receptor gene expression. We propose that the frequent loss of Dab2 during the onset of cancer enables a higher level of nuclear myosin VI activity, thereby driving the activity of the estrogen receptor to promote tumourgenesis.

cell biology↗