The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform
Bernd Wissinger - One of the best experts on this subject based on the ideXlab platform.
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foveal therapy in blue cone Monochromacy predictions of visual potential from artificial intelligence
Frontiers in Neuroscience, 2020Co-Authors: Alexander Sumaroka, Susanne Kohl, Bernd Wissinger, Artur V. Cideciyan, Rebecca Sheplock, Vivian Wu, Samuel G JacobsonAbstract:Novel therapeutic approaches for treating inherited retinal degenerations (IRDs) prompt a need to understand which patients with impaired vision have the anatomical potential to gain from participation in a clinical trial. We used supervised machine learning to predict foveal function from foveal structure in blue cone Monochromacy (BCM), an X-linked congenital cone photoreceptor dysfunction secondary to mutations in the OPN1LW/OPN1MW gene cluster. BCM patients with either disease-associated large deletion or missense mutations were studied and results compared with those from subjects with other forms of IRD and various degrees of preserved central structure and function. A machine learning technique was used to associate foveal sensitivities and best-corrected visual acuities to foveal structure in IRD patients. Two random forest models trained on IRD data were applied to predict foveal function in BCM. A curve fitting method was also used and results compared with those of the random forest models. The BCM and IRD patients had a comparable range of foveal structure. IRD patients had peak sensitivity at the fovea. Machine learning could successfully predict foveal sensitivity results from segmented or un-segmented optical coherence tomography input. Application of machine learning predictions to BCM at the fovea showed differences between predicted and measured sensitivities, thereby defining treatment potential. The curve fitting method provided similar results. Given a measure of visual acuity and foveal outer nuclear layer thickness, the question of how many lines of acuity would represent the best efficacious result for each BCM patient could be answered. We propose that foveal vision improvement potential in BCM is predictable from retinal structure using machine learning and curve fitting approaches. This should allow estimates of maximal efficacy in patients being considered for clinical trials and also guide decisions about dosing.
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blue cone Monochromacy caused by the c203r missense mutation or large deletion mutations
Investigative Ophthalmology & Visual Science, 2018Co-Authors: Alexander Sumaroka, Susanne Kohl, Artur V. Cideciyan, Alejandro J. Roman, Jason Charng, Alexandra V Garafalo, Windy Choi, Supna Saxena, Valeryia Aksianiuk, Bernd WissingerAbstract:Purpose: To compare the phenotype of blue cone Monochromacy (BCM) caused by large deletion mutations with those having the C203R missense mutation. Methods: BCM patients with large deletion mutations (n = 21; age range, 5-60 years), and with the C203R missense mutation (n = 13; age range, 5-70 years), were studied with optical coherence tomography, visual acuity, and perimetric sensitivity in a retrospective observational case series. Perceptual estimates of spatial resolution driven by rods, S-cones, and L/M-cones were obtained by the choice of chromatic gratings presented on varied adapting conditions with a modified microperimeter. Results: Both genotypes had abnormal foveal photoreceptor structure early in life. Patients with the C203R mutation, however, had decades-longer persistence of foveal photoreceptor outer nuclear layer thickness and a slower rate of development of inner segment/outer segment defects than did patients with large deletion mutations. At late ages, both genotypes had comparably severe losses of central structure. At the rod-rich hot spot, there was no difference in structure between cohorts with age. Grating acuities in all BCM patients were driven by S-cones and rods; the foveal structural differences were not reflected in a difference between cohorts in visual sensitivity and spatial resolution. Conclusions: A difference in structural phenotype due to the C203R mutation versus large deletion mutations in BCM was detected as a more prolonged persistence of foveal photoreceptor structure in patients with the missense mutation. This should be taken into account in planning natural history studies, selecting outcomes for clinical trials, and defining the time window for possible therapies.
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a 73 128 bp de novo deletion encompassing the opn1lw opn1mw gene cluster in sporadic blue cone Monochromacy a case report
BMC Medical Genetics, 2018Co-Authors: Elena Buenaatienza, Susanne Kohl, Fadi Nasser, Bernd WissingerAbstract:Blue Cone Monochromacy (BCM) is a rare congenital cone dysfunction disorder with X-linked recessive mode of inheritance. BCM is caused by mutations at the OPN1LW/MW cone opsin gene cluster including deletions of the locus control region (LCR) and/or parts of the gene cluster. We aimed at investigating the clinical presentation, genetic cause and inheritance underlying a sporadic case of BCM. We report a 24-year-old male presenting with congenital photophobia, nystagmus and colour vision abnormalities. There was no history of retinal dystrophy in the family. Clinical diagnosis of BCM was supported by genetic investigations of the patient and his family members. Molecular genetic analysis of the OPN1LW/OPN1MW gene cluster revealed a novel deletion of about 73 kb in the patient encompassing the LCR. The deletion was absent in the X-chromosomes of both the mother and transmitting grandfather. The present report provides the clinical findings and the genetic basis underlying a sporadic BCM case which is caused by a de novo deletion within the OPN1LW/MW gene cluster originating from the mother’s germline due to Alu-repeat mediated recombination. This is the first report of a de novo deletion resulting in BCM, highlighting the importance to consider BCM and perform genetic testing for this condition in male patients with cone dysfunction also in the absence of a positive family history.
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A 73,128 bp de novo deletion encompassing the OPN1LW/OPN1MW gene cluster in sporadic Blue Cone Monochromacy: a case report
BMC Medical Genetics, 2018Co-Authors: Elena Buena-atienza, Susanne Kohl, Fadi Nasser, Bernd WissingerAbstract:Blue Cone Monochromacy (BCM) is a rare congenital cone dysfunction disorder with X-linked recessive mode of inheritance. BCM is caused by mutations at the OPN1LW/MW cone opsin gene cluster including deletions of the locus control region (LCR) and/or parts of the gene cluster. We aimed at investigating the clinical presentation, genetic cause and inheritance underlying a sporadic case of BCM. We report a 24-year-old male presenting with congenital photophobia, nystagmus and colour vision abnormalities. There was no history of retinal dystrophy in the family. Clinical diagnosis of BCM was supported by genetic investigations of the patient and his family members. Molecular genetic analysis of the OPN1LW/OPN1MW gene cluster revealed a novel deletion of about 73 kb in the patient encompassing the LCR. The deletion was absent in the X-chromosomes of both the mother and transmitting grandfather. The present report provides the clinical findings and the genetic basis underlying a sporadic BCM case which is caused by a de novo deletion within the OPN1LW/MW gene cluster originating from the mother’s germline due to Alu-repeat mediated recombination. This is the first report of a de novo deletion resulting in BCM, highlighting the importance to consider BCM and perform genetic testing for this condition in male patients with cone dysfunction also in the absence of a positive family history.
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Blue cone nonochromacy gene mutation in Asia: phenotype variability
Acta Ophthalmologica, 2010Co-Authors: Pierre Bitoun, Susanne Kohl, F Rigaudiere, M. Papke, Bernd WissingerAbstract:Purpose A far East asian family with 4 affected maternal cousin males with congenital nystagmus, low vision and dyschromatopsia was investigated for a genetic cause after informed consent. Blue cone Monochromacy is a rare form of X-linked visual handicap with dyschromatopsia. Methods Family members had ophthalmologic examination including visual acuity, fundoscopy , slit lamp, biomicroscopy,colour vision testing and ERG and VEP recordings.DNA analysis of the composition of the cone ospin gene cluster was performed by PCR and PCR/RFLP as well as direct sequencing of LWS opsin gene. Results A novel nonsense Mutation in the single Long wave sensitive opsin gene was identified in all affected males and carrier females. The variability of the phenotype as well as the added role of parental myopia transmission in the phenotype will be discussed. Conclusion This is the first reported molecular diagnosis of blue cone Monochromacy in the Asian population.The compound effect of dominantly inherited myopia offers insight of the effect of the added mutational load in these patients.
James R Lupski - One of the best experts on this subject based on the ideXlab platform.
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Achromatopsia: the CNGB3 p.T383fsX mutation results from a founder effect and is responsible for the visual phenotype in the original report of uniparental disomy 14
Human Genetics, 2007Co-Authors: Wojciech Wiszniewski, Richard Alan Lewis, James R LupskiAbstract:Achromatopsia (ACHM) or rod Monochromacy is an autosomal recessive and genetically heterogeneous retinal disorder. It is characterized by a lack of color discrimination, poor visual acuity, photodysphoria, pendular infantile nystagmus, and abnormal photopic electroretinographic (ERG) recordings with preservation of rod-mediated function. Mutations in three known genes are causative; including genes for the α and β subunits of the cyclic nucleotide-gated cation channel ( CNGA3 and CNGB3 , respectively) and cone photoreceptor transducin— GNAT2. We investigated the prevalence of mutations in achromatopsia-causing genes in a cohort of 16 families with both clinical and electrophysiologic evidence consistent with autosomal recessive transmission, including one subject with achromatopsia and maternal isodisomy for chromosome 14. The most frequent mutation, p.T383fsX in CNGB3 , accounted for 75% (18/24) of disease-associated alleles; intragenic SNPs in unrelated patients revealed transmission of a common haplotype consistent with a founder effect. Homozygous p.T383fsX mutation in CNGB3 that maps to chromosome 8 was detected in a patient with achromatopsia and systemic features associated with uniparental disomy (UPD) of chromosome 14. Two novel variants, p.R223G and p.A621E were found in CNGA3 . We conclude that CNGA3 and CNGB3 mutations are responsible for the substantial majority of achromatopsia. Furthermore, the CNGB3 mutation p.T383fsX is a predominant mutation, results from a founder effect, and is responsible for the ACHM in the original clinical report of UPD 14.
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Achromatopsia: the CNGB3 p.T383fsX mutation results from a founder effect and is responsible for the visual phenotype in the original report of uniparental disomy 14.
Human genetics, 2007Co-Authors: Wojciech Wiszniewski, Richard Alan Lewis, James R LupskiAbstract:Achromatopsia (ACHM) or rod Monochromacy is an autosomal recessive and genetically heterogeneous retinal disorder. It is characterized by a lack of color discrimination, poor visual acuity, photodysphoria, pendular infantile nystagmus, and abnormal photopic electroretinographic (ERG) recordings with preservation of rod-mediated function. Mutations in three known genes are causative; including genes for the alpha and beta subunits of the cyclic nucleotide-gated cation channel (CNGA3 and CNGB3, respectively) and cone photoreceptor transducin--GNAT2. We investigated the prevalence of mutations in achromatopsia-causing genes in a cohort of 16 families with both clinical and electrophysiologic evidence consistent with autosomal recessive transmission, including one subject with achromatopsia and maternal isodisomy for chromosome 14. The most frequent mutation, p.T383fsX in CNGB3, accounted for 75% (18/24) of disease-associated alleles; intragenic SNPs in unrelated patients revealed transmission of a common haplotype consistent with a founder effect. Homozygous p.T383fsX mutation in CNGB3 that maps to chromosome 8 was detected in a patient with achromatopsia and systemic features associated with uniparental disomy (UPD) of chromosome 14. Two novel variants, p.R223G and p.A621E were found in CNGA3. We conclude that CNGA3 and CNGB3 mutations are responsible for the substantial majority of achromatopsia. Furthermore, the CNGB3 mutation p.T383fsX is a predominant mutation, results from a founder effect, and is responsible for the ACHM in the original clinical report of UPD 14.
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maternal uniparental isodisomy of chromosome 14 association with autosomal recessive rod Monochromacy
American Journal of Human Genetics, 1992Co-Authors: Liu Pentao, R A Lewis, David H Ledbetter, Pragna Patel, James R LupskiAbstract:Rod Monochromacy (complete congenital achromatopsia) is inherited as an autosomal recessive trait of unknown genetic location. The disorder is characterized by total absence of color discrimination because retinal cone photoreceptors do not develop; systemic features do not occur. A 20-year-old white female with rod Monochromacy presented with short stature (less than 5th percentile), mild developmental delay, premature puberty, small hands and feet (length less than 5th percentile), minimal dysmorphism, and a reproductive history of three consecutive first-trimester miscarriages. Cytogenetic analysis showed 45,XX,rob(14;14) in all 30 cells examined. Southern analysis of DNA from the patient and her phenotypically normal mother and two brothers (her father is deceased) ascertained the parental origin of the 14;14 Robertsonian translocation. Analysis of RFLPs associated with nine VNTR probes and two dinucleotide repeat polymorphisms from chromosome 14 demonstrated that the patient had inherited two copies of a single allele, each of which was maternally derived. A fully informative RFLP analysis of three probes from chromosome 14 enabled reconstruction of the paternal haplotype and showed the lack of any paternal contribution to the subject. These data are consistent with maternal isodisomy for all portions of chromosome 14 tested by these markers. This finding suggests that rod Monochromacy maps to chromosome 14, and it emphasizes the importance of uniparental isodisomy to provide a putative chromosomal assignment of a gene for a rare autosomal recessive disorder.
Susanne Kohl - One of the best experts on this subject based on the ideXlab platform.
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Genetics of color vision deficiencies.
Developments in ophthalmology, 2020Co-Authors: Samir S. Deeb, Susanne KohlAbstract:: The normal X-chromosome-linked color vision gene array is composed of a single red pigment gene followed by one or more green pigment genes. The high degree of homology between these genes predisposed them to unequal recombination, leading to gene deletions or the formation of red-green hybrid genes that explain the majority of the common red-green color vision deficiencies. Gene expression studies suggest that only the two most proximal genes of the array are expressed in the retina. The severity of the color vision defect is roughly related to the difference in absorption maxima of the photopigments encoded by the first two genes of the array. A single amino acid polymorphism (Ser180Ala) in the red pigment accounts for the subtle difference in normal color vision and influences the severity of color vision deficiency. Blue cone Monochromacy is a rare disorder that involves absence of red and green cone function. It is caused either by deletion of a critical region that regulates expression of the red/green gene array, or by mutations that inactivate the red and green pigment genes. Total color blindness is another rare disease that involves complete absence of all cone function. A number of mutations in the genes encoding the cone-specific alpha- and beta-subunits of the cation channel and the alpha-subunit of transducin have been implicated in this disorder.
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foveal therapy in blue cone Monochromacy predictions of visual potential from artificial intelligence
Frontiers in Neuroscience, 2020Co-Authors: Alexander Sumaroka, Susanne Kohl, Bernd Wissinger, Artur V. Cideciyan, Rebecca Sheplock, Vivian Wu, Samuel G JacobsonAbstract:Novel therapeutic approaches for treating inherited retinal degenerations (IRDs) prompt a need to understand which patients with impaired vision have the anatomical potential to gain from participation in a clinical trial. We used supervised machine learning to predict foveal function from foveal structure in blue cone Monochromacy (BCM), an X-linked congenital cone photoreceptor dysfunction secondary to mutations in the OPN1LW/OPN1MW gene cluster. BCM patients with either disease-associated large deletion or missense mutations were studied and results compared with those from subjects with other forms of IRD and various degrees of preserved central structure and function. A machine learning technique was used to associate foveal sensitivities and best-corrected visual acuities to foveal structure in IRD patients. Two random forest models trained on IRD data were applied to predict foveal function in BCM. A curve fitting method was also used and results compared with those of the random forest models. The BCM and IRD patients had a comparable range of foveal structure. IRD patients had peak sensitivity at the fovea. Machine learning could successfully predict foveal sensitivity results from segmented or un-segmented optical coherence tomography input. Application of machine learning predictions to BCM at the fovea showed differences between predicted and measured sensitivities, thereby defining treatment potential. The curve fitting method provided similar results. Given a measure of visual acuity and foveal outer nuclear layer thickness, the question of how many lines of acuity would represent the best efficacious result for each BCM patient could be answered. We propose that foveal vision improvement potential in BCM is predictable from retinal structure using machine learning and curve fitting approaches. This should allow estimates of maximal efficacy in patients being considered for clinical trials and also guide decisions about dosing.
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blue cone Monochromacy caused by the c203r missense mutation or large deletion mutations
Investigative Ophthalmology & Visual Science, 2018Co-Authors: Alexander Sumaroka, Susanne Kohl, Artur V. Cideciyan, Alejandro J. Roman, Jason Charng, Alexandra V Garafalo, Windy Choi, Supna Saxena, Valeryia Aksianiuk, Bernd WissingerAbstract:Purpose: To compare the phenotype of blue cone Monochromacy (BCM) caused by large deletion mutations with those having the C203R missense mutation. Methods: BCM patients with large deletion mutations (n = 21; age range, 5-60 years), and with the C203R missense mutation (n = 13; age range, 5-70 years), were studied with optical coherence tomography, visual acuity, and perimetric sensitivity in a retrospective observational case series. Perceptual estimates of spatial resolution driven by rods, S-cones, and L/M-cones were obtained by the choice of chromatic gratings presented on varied adapting conditions with a modified microperimeter. Results: Both genotypes had abnormal foveal photoreceptor structure early in life. Patients with the C203R mutation, however, had decades-longer persistence of foveal photoreceptor outer nuclear layer thickness and a slower rate of development of inner segment/outer segment defects than did patients with large deletion mutations. At late ages, both genotypes had comparably severe losses of central structure. At the rod-rich hot spot, there was no difference in structure between cohorts with age. Grating acuities in all BCM patients were driven by S-cones and rods; the foveal structural differences were not reflected in a difference between cohorts in visual sensitivity and spatial resolution. Conclusions: A difference in structural phenotype due to the C203R mutation versus large deletion mutations in BCM was detected as a more prolonged persistence of foveal photoreceptor structure in patients with the missense mutation. This should be taken into account in planning natural history studies, selecting outcomes for clinical trials, and defining the time window for possible therapies.
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a 73 128 bp de novo deletion encompassing the opn1lw opn1mw gene cluster in sporadic blue cone Monochromacy a case report
BMC Medical Genetics, 2018Co-Authors: Elena Buenaatienza, Susanne Kohl, Fadi Nasser, Bernd WissingerAbstract:Blue Cone Monochromacy (BCM) is a rare congenital cone dysfunction disorder with X-linked recessive mode of inheritance. BCM is caused by mutations at the OPN1LW/MW cone opsin gene cluster including deletions of the locus control region (LCR) and/or parts of the gene cluster. We aimed at investigating the clinical presentation, genetic cause and inheritance underlying a sporadic case of BCM. We report a 24-year-old male presenting with congenital photophobia, nystagmus and colour vision abnormalities. There was no history of retinal dystrophy in the family. Clinical diagnosis of BCM was supported by genetic investigations of the patient and his family members. Molecular genetic analysis of the OPN1LW/OPN1MW gene cluster revealed a novel deletion of about 73 kb in the patient encompassing the LCR. The deletion was absent in the X-chromosomes of both the mother and transmitting grandfather. The present report provides the clinical findings and the genetic basis underlying a sporadic BCM case which is caused by a de novo deletion within the OPN1LW/MW gene cluster originating from the mother’s germline due to Alu-repeat mediated recombination. This is the first report of a de novo deletion resulting in BCM, highlighting the importance to consider BCM and perform genetic testing for this condition in male patients with cone dysfunction also in the absence of a positive family history.
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A 73,128 bp de novo deletion encompassing the OPN1LW/OPN1MW gene cluster in sporadic Blue Cone Monochromacy: a case report
BMC Medical Genetics, 2018Co-Authors: Elena Buena-atienza, Susanne Kohl, Fadi Nasser, Bernd WissingerAbstract:Blue Cone Monochromacy (BCM) is a rare congenital cone dysfunction disorder with X-linked recessive mode of inheritance. BCM is caused by mutations at the OPN1LW/MW cone opsin gene cluster including deletions of the locus control region (LCR) and/or parts of the gene cluster. We aimed at investigating the clinical presentation, genetic cause and inheritance underlying a sporadic case of BCM. We report a 24-year-old male presenting with congenital photophobia, nystagmus and colour vision abnormalities. There was no history of retinal dystrophy in the family. Clinical diagnosis of BCM was supported by genetic investigations of the patient and his family members. Molecular genetic analysis of the OPN1LW/OPN1MW gene cluster revealed a novel deletion of about 73 kb in the patient encompassing the LCR. The deletion was absent in the X-chromosomes of both the mother and transmitting grandfather. The present report provides the clinical findings and the genetic basis underlying a sporadic BCM case which is caused by a de novo deletion within the OPN1LW/MW gene cluster originating from the mother’s germline due to Alu-repeat mediated recombination. This is the first report of a de novo deletion resulting in BCM, highlighting the importance to consider BCM and perform genetic testing for this condition in male patients with cone dysfunction also in the absence of a positive family history.
Nathan Scott Hart - One of the best experts on this subject based on the ideXlab platform.
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cone Monochromacy and visual pigment spectral tuning in wobbegong sharks
Biology Letters, 2012Co-Authors: Susan Michelle Theiss, Shaun Patrick Collin, Wayne I L Davies, David Hunt, Nathan Scott HartAbstract:Much is known regarding the evolution of colour vision in nearly every vertebrate class, with the notable exception of the elasmobranchs. While multiple spectrally distinct cone types are found in some rays, sharks appear to possess only a single class of cone and, therefore, may be colour blind. In this study, the visual opsin genes of two wobbegong species, Orectolobus maculatus and Orectolobus ornatus, were isolated to verify the molecular basis of their Monochromacy. In both species, only two opsin genes are present, RH1 (rod) and LWS (cone), which provide further evidence to support the concept that sharks possess only a single cone type. Examination of the coding sequences revealed substitutions that account for interspecific variation in the photopigment absorbance spectra, which may reflect the difference in visual ecology between these species.
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Microspectrophotometric evidence for cone Monochromacy in sharks
Naturwissenschaften, 2011Co-Authors: Nathan Scott Hart, Susan Michelle Theiss, Blake Kristin Harahush, Shaun Patrick CollinAbstract:Sharks are apex predators, and their evolutionary success is in part due to an impressive array of sensory systems, including vision. The eyes of sharks are well developed and function over a wide range of light levels. However, whilst close relatives of the sharks—the rays and chimaeras—are known to have the potential for colour vision, an evolutionary trait thought to provide distinct survival advantages, evidence for colour vision in sharks remains equivocal. Using single-receptor microspectrophotometry, we measured the absorbance spectra of visual pigments located in the retinal photoreceptors of 17 species of shark. We show that, while the spectral tuning of the rod (wavelength of maximum absorbance, λ_max 484–518 nm) and cone (λ_max 532–561 nm) visual pigments varies between species, each shark has only a single long-wavelength-sensitive cone type. This suggests that sharks may be cone monochromats and, therefore, potentially colour blind. Whilst cone Monochromacy on land is rare, it may be a common strategy in the marine environment: many aquatic mammals (whales, dolphins and seals) also possess only a single, green-sensitive cone type. It appears that both sharks and marine mammals may have arrived at the same visual design by convergent evolution. The spectral tuning of the rod and cone pigments of sharks is also discussed in relation to their visual ecology.
Shaun Patrick Collin - One of the best experts on this subject based on the ideXlab platform.
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cone Monochromacy and visual pigment spectral tuning in wobbegong sharks
Biology Letters, 2012Co-Authors: Susan Michelle Theiss, Shaun Patrick Collin, Wayne I L Davies, David Hunt, Nathan Scott HartAbstract:Much is known regarding the evolution of colour vision in nearly every vertebrate class, with the notable exception of the elasmobranchs. While multiple spectrally distinct cone types are found in some rays, sharks appear to possess only a single class of cone and, therefore, may be colour blind. In this study, the visual opsin genes of two wobbegong species, Orectolobus maculatus and Orectolobus ornatus, were isolated to verify the molecular basis of their Monochromacy. In both species, only two opsin genes are present, RH1 (rod) and LWS (cone), which provide further evidence to support the concept that sharks possess only a single cone type. Examination of the coding sequences revealed substitutions that account for interspecific variation in the photopigment absorbance spectra, which may reflect the difference in visual ecology between these species.
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Microspectrophotometric evidence for cone Monochromacy in sharks
Naturwissenschaften, 2011Co-Authors: Nathan Scott Hart, Susan Michelle Theiss, Blake Kristin Harahush, Shaun Patrick CollinAbstract:Sharks are apex predators, and their evolutionary success is in part due to an impressive array of sensory systems, including vision. The eyes of sharks are well developed and function over a wide range of light levels. However, whilst close relatives of the sharks—the rays and chimaeras—are known to have the potential for colour vision, an evolutionary trait thought to provide distinct survival advantages, evidence for colour vision in sharks remains equivocal. Using single-receptor microspectrophotometry, we measured the absorbance spectra of visual pigments located in the retinal photoreceptors of 17 species of shark. We show that, while the spectral tuning of the rod (wavelength of maximum absorbance, λ_max 484–518 nm) and cone (λ_max 532–561 nm) visual pigments varies between species, each shark has only a single long-wavelength-sensitive cone type. This suggests that sharks may be cone monochromats and, therefore, potentially colour blind. Whilst cone Monochromacy on land is rare, it may be a common strategy in the marine environment: many aquatic mammals (whales, dolphins and seals) also possess only a single, green-sensitive cone type. It appears that both sharks and marine mammals may have arrived at the same visual design by convergent evolution. The spectral tuning of the rod and cone pigments of sharks is also discussed in relation to their visual ecology.