Evolution and genetics of colour vision Flashcards
Colour appearance and wavelength composition are dissociable. Explain.
- Colour constancy shows that wavelength can change while colour appearance remains constant
- Simultaneous colour contrast shows that colour appearance can change even though wavelength remains constant
- Opponent pressing along retinogeniculate pathway seems suited to signal wavelength composition of light
- Perhaps further cortical processing is required to account for perceived colour e.g. colour constancy
DORSAL stream: ?
-where?
Onward connections via MT to parietal areas crucial for visually guided action
VENTRAL stream: ?
-what?
Onward connections via V4 to temporal areas crucial for visual recognition
Cortical processing of colour
- Initial reports suggested colour-sensitive cells confined to blobs in V1
- Circular RFs, no orientation sensitivity
- Orientation sensitivity, no colour sensitivity in interblobs
- Later work cast doubt
- Onward connections maintained segregation to specialised colour processing areas
Is V4 specialised for colour?
- Fourth visual area (Zeki, 1971) discovered from orderly projections from V2, V3
- Early recordings hinted at specialisation for colour
- was sometimes discussed as ‘the colour centre’
- Zeki classified cells as wavelength coding to colour coding in monkey visual cortex; found only wavelength in V1 but some in V4 were colour coding
- However, V4 lesions had little effect on colour vision and greater effect on shape discrimination
- V4 may be involved in colour processing but it’s not ‘the cortical colour centre’ (no evidence)
Colour coding vs wavelength coding cells
- Wavelength and colour are dissociated - responses of colour cells would correlate with perceived colour, while wavelength cells would correlate with wavelength composition
- Zeki (1980, 1983) found only wavelength cells in V1 but significant proportion of colour sensitive in V4
Explain the difference between single opponent and double opponent cells
SINGLE:
-opposed inputs based on wavelength e.g. parvocellular in LGN
-could contribute to colour constancy
DOUBLE:
-opposed inputs based on both wavelength and spatial location in RF
-could contribute to colour constancy
-originally reported in V1 blobs - circular RFs without orientation sensitivity
-later reports questioned they existence
-recent evi suggests DO cells are found in V1 but not confined to blobs and have oriented RFs
describe Visual pigments
- Photon-absorbing molecules that enable photoreceptors to produce electrical signals in response to light
- consists of an opsin bound with a chromophore
- opsins are members of the GPCR superfamily
- light sensitivity is conferred by the absorption of a photon by the chromophore and subsequent conformational change (11-cis retinal to trans retinal)
- Spectral sensitivity is conferred by the AA sequence of the opsin (determined by opsin)
- Likelihood of absorbing photons of different energy/wavelength is determined by oxygen
Sequence analysis suggests 5 vertebrate opsin families. Distinguish between cone and rod opsins
- cone opsins very ancient ~ 540 MYA
- rod opsin family emerges after divergence of cone opsins
how many opsin family cone vs rod
4 cone opsin families and 1 rod opsin family
describe Spectral tuning of opsin gene families
- each opsin within a family can be tuned by AA substitutions
- peak spectral sensitivity can be shifted (by a few nm) by single AA substitutions at certain key positions
Mammalian opsin families
- The base mammalian condition is dichromatic
- modern mammals (eutharians) have retained the rod opsin and two of the cone opsins
- a recent (~30 MYA) duplication of the LWS gene in African primates diverged to give the M and L cone opsins (both members of the ancestral LWS family)
Cerebral achromatopsia
- Rare condition associated with damage to ventral visual areas
- does not depend o damage to V1
- includes homologues of monkey extrastriate ventral stream areas including V4
- usually complicated with associated deficits in object perceptions
- complete loss of colour sensations but normal acuity
- patients can detect borders defined only by chromaticity (not luminance) indicating intact wavelength discrimination despite loss of colour
Mammalian LWS opsin gene is on the ?
x-chromosome
- old world primates (catarrhine) have two similar genes head to tail (M and L opsins)
- thought that duplication of original LWS opsin gene followed by divergence (<5 AA substitution) gave rise to distinct M and L opsins
- LCR (randomly) activates promoter of L or M opsins - only one expressed in a single cone
Genetics of human opsins
- two AA substitutions in exon 5 account for most of the spectral difference between human M and L opsins
- substitutions in other positions confer allelic variation such that the peak sensitivity of M and L can vary by a few nm across individuals
Human colour deficiencies
- Dichromat
- single X chromosome (in males) has only M or L genes
- cone sensitivities:
- S, M (protanope)
- S, L (deuteranope)
- Anomalous trichromat
- allelic copies of M or L genes
- S, M, M’ (protanomalous)
- S, L, L’ (deuteranomalous)
Could centre-surround organisation in the retina exploit the emergence of a new spectral class of cone?
- Ancient subsystem: S-cone opposed with single class of M/L cone supports dichromatic colour vision
- recent subsystem: antagonistic inputs to centre and surround from single class of M/L cone
- divergence of M/L into distinct M and L cones means centre and surround will have spectrally opponent inputs
Polymorphic colour vision in new-world primates
- old-world primates (including humans) are trichromats (A)
- new-world primates are dichromats (B,C) but in several species LWS opsin gene comes in 3 alleles with sensitivity similar to human M, L or intermediate
- males are homozygous females are dichromats
- heterozygous females are trichromats (depends on X-inactivation; allelic gene from only one of the X-chromosomes is expressed)
Implications with polymorphic colour vision?
- possible scenario for evolution of trichromacy in human lineage (old-world primates)
- if a gene for a new class of photoreceptor evolves, do we also need genes to modify the circuitry it feeds into? or is the nervous system flexible enough to exploit it straight away?
- is early developmental experience needed to ensure a new photoreceptor can work with existing circuitry?
Genetic engineering of trichomacy in dichromatic male monkeys
- squirrel monkeys (new world, heterozygous female trichromats (S/M/L), males and homozygous females dichromate (S/M)
- transfected adult males with recombinant human L opsin
- behavioural demonstration of red-green colour discrimination after 20 weeks (coinciding with significan levels of transgene expression)
- adult CNS is sufficiently plastic to exploit new spectral cone class with existing circuitry
