silver in cat.pdf

Journal of Heredity Advance Access published April 27, 2009

Journal of Heredity

doi:10.1093/jhered/esp018

For permissions, please email: journals.permissions@oxfordjournals.org.

Mapping of the Domestic Cat ‘‘SILVER’’

Coat Color Locus Identiﬁes a Unique

Genomic Location for Silver in Mammals

M ARILYN M ENOTTI -R AYMOND ,V ICTOR A. D AVID ,E DUARDO E IZIRIK ,M ELODY E. R OELKE ,H ELYA G HAFFARI ,

AND S TEPHEN J. O’B RIEN

From the Laboratory of Genomic Diversity, National Cancer Institute-Frederick, Frederick, MD 21702 (Menotti-Raymond,

David, Ghaffari, and O’Brien); the Centro de Biologia, Gen ˆ mica e Molecular, Faculdade de Biociˆncias, PUCRS, Porto

Alegre, RS 90619-900, Brazil (Eizirik); the Instituto Pr ´ -Carn´voros, Brazil (Eizirik); and the Laboratory of Genomic Diversity,

SAIC-Frederick, National Cancer Institute-Frederick, Frederick, MD 21702 (Roelke).

Address correspondence to Marilyn Menotti-Raymond at the address above, or e-mail: raymond@ncifcrf.gov.

Abstract

The SILVER locus has been mapped in the domestic cat, identifying a unique genomic location distinct from that of any

known reported gene associated with silver or hypopigmentation in mammals. A demonstrated lack of linkage to SILV, the

strong candidate gene for silver, led to the initiation of a genome scan utilizing 2 pedigrees segregating for silver coat color.

Linkage mapping deﬁned a genomic region for SILVER as a 3.3-Mb region, (95.87–99.21 Mb) on chromosome D2, (peak

logarithm of the odds 5 10.5, h 5 0), which displays conserved synteny to a genomic interval between 118.58 and

121.85 Mb on chromosome 10 in the human genome. In the domestic cat, mutations at the SILVER locus suppress the

development of pigment in the hair, but in contrast to other mammalian silver variants, there is an apparently greater

inﬂuence on the production of pheomelanin than eumelanin pigment. The mapping of a novel locus for SILVER offers

much promise in identifying a gene that may help elucidate aspects of pheomelanogenesis, a pathway that has been very

elusive, and illustrates the promise of the cat genome project in increasing our understanding of basic biological processes of

general relevance for mammals.

Key words:

coat color, domestic cat, genetic linkage mapping, pheomelanogenic, SILVER

It is estimated that the cat was domesticated approximately

10 000 years ago (Vigne et al. 2004) in the Middle East

(Driscoll et al. 2007), likely as a consequence of the

development of the ﬁrst villages and the storage of wild

grain stocks which attracted an abundant source of rodents.

This wild progenitor of the domestic cat, Felis silvestris lybica,

the African wild cat, is difﬁcult to distinguish today from

a common domestic tabby cat with mackerel stripes set

against a wild-type agouti coat background (Figure 1). Since

domestication, a wide range of coat color and pattern

variants have arisen in the domestic cat, which have not

been reported in the wild cat, including a variety of coat

colors, distinctive hair phenotypes, as well as coat patterns

(stripes, spots, and blotches, including the unpatterned coat

of the ‘‘ticked tabby’’). This development of pelage

polymorphism has been observed in most mammals which

have experienced domestication, partly as a consequence of

release from purifying selection in natural populations but

also due to intense artiﬁcial selection in favor of color

morphs or patterns that were pleasing to humans (Zeuner

1963; Trut 1999).

With the development of genomic resources in the

domestic cat, including comprehensive genetic and radiation

hybrid maps (Menotti-Raymond et al. 1999, 2003, 2009;

Murphy et al. 2000, 2007; Davis et al. 2009; Schmidt-

K ¨ ntzel et al. 2009), a 1.9 whole-genome sequence draft

(Pontius et al. 2007), and an interactive web browser

(Pontius and O’Brien 2007), several of the genes underlying

this phenotypic variation have been mapped and/or

characterized at a molecular genetic level, including black

(Eizirik et al. 2003), brown, and cinnamon (Schmidt-

K¨ntzel et al. 2005), dilute (Ishida et al. 2006), Siamese,

and Burmese phenotypes, albino (Lyons et al. 2005; Imes

et al. 2006), long hair (Drogemuller et al. 2007; Kehler et al.

2007), and orange (Schmidt-K ¨ ntzel et al. 2009).

The cat displays additional color morphs, which have not

yet been mapped or characterized, including a silver pelage

variant (Figure 1), which is due to the autosomal dominant

Journal of Heredity

Figure 1.

Images of a wild cat (right), Felis silvestris lybica, and the silver male Ocicat used in the generation of Pedigree Two.

action of what has been termed the ‘‘Inhibitor’’ locus (Vella

et al. 1999). In the domestic cat, mutations at the Inhibitor

or SILVER locus suppress the development of pigment in

the hair, but in contrast to other mammalian silver variants,

there is an apparently greater inﬂuence on the production of

pheomelanin than eumelanin pigment (Vella et al. 1999).

The characteristic ‘‘yellowish-orange’’ agouti band seen in

wild-type cats, resulting from a shift in eumelanin to

pheomelanin production (Eizirik et al. 2003), is nearly white

or colorless in silver cats. Further, hairs in silver domestic

cats display a silver (near colorless) base, with normal

(including eumelanic, depending on other loci) pigmentation

observed in the hair tips (Figure 2). A striking silver

phenotype in the cat is ‘‘smoke,’’ which stems from the

effect of silver on a nonagouti (melanistic, i.e., black)

background. The guard hairs in these cats display a silver

base, with lengthened black tips, as compared with hairs in

silver cats (Vella et al. 1999) (Figure 2). SILVER does not

prevent the synthesis of pheomelanic pigments, as witnessed

in orange, silver tabbies. However, the color of the orange

pigmentation is somewhat different than observed in an

orange, non-silver cat, being devoid of the warm brown

tones seen in a classic orange cat (Pﬂueger S, personal

communication).

A SILVER locus was ﬁrst described in the mouse by

Dunn and Thigpen (1930). Since then, genetic loci

producing silver, or hypopigmentation phenotypes, have

been reported in a number of organisms, including horses,

dogs, cattle, mice, birds, chickens, and zebra ﬁsh (Martinez-

Esparza et al. 1999; Kerje et al. 2004; Schonthaler et al.

2005; Brunberg et al. 2006; Clark et al. 2006; K ¨ hn and

Weikard 2007; Reissmann et al. 2007). The gene implicated

in these ‘‘silver’’ phenotypes has been the SILV locus

(also known as ‘‘silver homolog’’ or PMEL17), which

generates a protein product important in early stages of

melanosome biogenesis (Kobayashi et al. 1994; Zhou et al.

1994; Berson et al. 2001). The mode of inheritance is

typically autosomal dominant. In zebra ﬁsh and dogs,

defects in vision and hypopigmentation are associated with

mutations at the SILV locus (Schonthaler et al. 2005;

Clark et al. 2006). Dogs that carry the merle mutation,

characterized as an insertion of a short interspersed element

in SILV, exhibit patches of diluted pigment juxtaposed with

patches of normal coloration and additionally suffer from

auditory abnormalities (Clark et al. 2006). In humans, there

are no reported mutations associated with the SILV gene,

which is located on 12q13–q14. There are no reported

pathologies associated with the silver phenotype in cats.

Figure 2.

Panels demonstrate hairs from domestic cat silver (A), smoke (B), and melanistic (C) individuals.

Menotti-Raymond et al. Domestic Cat Mapping of the SILVER Locus

Figure 3. Pedigrees used for the mapping of the domestic cat SILVER locus; Pedigree One (left); Pedigree Two (right).

Male, heterozygous for SILVER;

female, heterozygous for SILVER.

Additional genes in mammals have been reported involved

in hypopigmentation (Mariat et al. 2003; Cook et al. 2008).

We report here the mapping of the SILVER locus in the

domestic cat identifying a new locus for silver/hypopig-

mentation in mammals.

a standard concentration of 2.5 ng/ll with sterile distilled

water (Quality Biological).

Polymerase chain reaction Ampliﬁcation and Genotyping of

Microsatellites

A genome scan was initiated using microsatellites selected at

regular intervals along the cat genome (Murphy et al. 2007;

Menotti-Raymond et al. 2009). Polymerase chain reaction

(PCR) ampliﬁcation of microsatellites was performed with

a touchdown PCR protocol as described previously

(Menotti-Raymond et al. 2005). Sample electrophoresis

and genotyping, as well as Mendelian inheritance checking,

were carried out as previously described (Ishida et al. 2006).

Materials and Methods

Animals

Two pedigrees were utilized (Figure 3). Pedigree One was

developed at the National Institutes of Health Animal Center

(NIHAC). The pedigree was founded with a purebred, silver

male cat of the Egyptian Mau breed, which was crossed with

3 unrelated non-silver outbred (they did not belong to a

registered breed) females. Seven progeny were produced, 5 of

which were silver, demonstrating that the parental male was

heterozygous for SILVER. These 5 F 1 individuals (4 females

and a male) were backcrossed to non-silver outbred cats,

producing a third-generation of 23 animals, 19 of which could

be conﬁdently phenotyped for the SILVER locus. Overall,

the F 1 and backcross individuals exhibited an approximate

1:1 ratio of silver (n 5 14) to non-silver (n 5 12) phenotypes.

Another pedigree (referred to as ‘‘Pedigree Two’’ henceforth)

that segregated for silver was provided by a cooperating cat

breeder. One silver male, a purebred Ocicat, was mated to

2 females producing 12 progeny, 5 of which were silver and

7 non-silver.

Development of Additional Microsatellites for Fine Mapping

of SILVER

After linkage with SILVER was established to a genomic

region using previously published cat microsatellites, addi-

tional markers from this candidate segment region were

mined from the cat 1.9 whole-genome sequence (Pontius

et al. 2007). Microsatellite markers, selected based on their

location on cat chromosome D2, were mined from the

GARFIELD cat genome browser ( http://lgd.abcc.ncifcrf.

gov/cgi-bin/gbrowse/cat/) (Pontius and O’Brien 2007).

These include all loci for SILVER mapping in Table 1 with

preﬁx ‘‘D2_.’’ Primers for new loci ( Supplementary material,

Appendix 1) were designed with Primer 3 ( http://frodo.wi.

mit.edu/cgi-bin/primer3/primer3_www.cgi) (Rozen and

Skaletsky 2000), including an M13 tail for ﬂuorescent labeling

of PCR products (Boutin-Ganache et al. 2001).

DNA Extraction

For all individuals from Pedigree One, blood samples were

collected as a standard source of DNA; in addition, skin

biopsies were collected from each animal according to

NIHAC animal protocols and cell lines were established as

a source of high-quality genomic material. Buccal swab

samples were supplied for individuals in Pedigree Two.

DNA was extracted from whole blood and ﬁbroblast cell

lines using a QIAamp DNA blood Midi or Mini Kit

(Qiagen) for blood or buccal samples, respectively, using

manufacturer’s protocols. DNA was quantiﬁed using

a Hoefer DNA Quant 200 Flurometer (Amersham

Biosciences). A proportion of each sample was diluted to

Genetic Linkage Mapping

Single-marker logarithm of the odds (LOD) scores were

computed, using Superlink (Fishelson and Geiger 2002,

2004), as described in Ishida et al. (2006) and Kehler et al.

(2007). Since the 2 pedigrees were established each from

a single male, one a purebred Egyptian Mau and the other

a purebred Ocicat, we analyzed the data both as a single

pedigree and as 2 independent pedigrees. SILVER mapped

to the same genomic region in both pedigrees (data

not shown).

Journal of Heredity

Table 1. Microsatellite markers utilized in mapping of SILVER

Marker a

Dog Chr 28 b

Human Chr 10 c

LOD

Cat Chr D2

FCA955

2.8

0.2

86,022,426

21,788,479

108,516,870

FCA1239

2.0

0.1

86,789,157

22,486,644

109,388,134

FCA1241

3.7

0.2

91,583,985

26,143,901

113,744,643

D2_93.3

3.4

0.05

93,358,579

28,191,399

116,105,982

D2_93.9

5.9

0.1

93,900,284

28,668,678

116,660,785

D2_94.5

6.2

0.1

94,524,844

29,257,166

117,375,668

D2_95.1

6.8

0.05

95,192,200

29,813,138

117,921,715

FCA954

5.8

0.05

95,823,888

30,338,383

118,536,757

FCA1240

7.4

0.05

95,875,325

30,384,390

118,588,972

D2_96.1

10.5

96,114,956

30,595,675

118,846,522

D2_96.9

8.1

96,990,099

31,332,116

119,656,273

D2_98.1

10.2

98,100,274

32,256,893

120,742,485

D2_98.6

7.8

98,601,083

32,659,233

121,227,619

D2_99.16

5.3

99,167,851

33,131,599

121,797,461

D2_99.21

6.7

0.05

99,219,025

33,175,512

121,850,894

D2_99.27

6.7

0.05

99,275,747

33,215,309

121,887,548

F41

5.1

0.1

99,706,534

33,563,419

122,318,976

FCA1242

1.9

0.1

105,677,501

38,419,330

127,982,490

FCA1243

0.6

0.3

107,394,183

39,793,387

129,659,013

a Markers in bold are previously published; other markers were mined from GARFIELD genome browser as described in the Materials and methods.

b Estimated by Blat genome search of 400 bp of cat genomic DNA ﬂanking sequence to Dog May 2005 assembly using the UCSC genome browser.

c Dog coordinates converted to the position on Human March 2006 assembly using the UCSC genome browser.

Results and Discussion

We began our analysis by genotyping a microsatellite marker

(FCA867, at 102.1 Mb on B4) closely linked to the strong

candidate locus for SILVER, the SILV gene on cat

chromosome B4, 96.37–96.39 Mb (Murphy et al. 2007). A

demonstrated lack of linkage between FCA867 and

SILVER (LOD 5 5.7, h 5 0), with a LOD score below

the frequently used exclusion criterion of 2 (Ott 1991), led

to the initiation of a genome scan using microsatellites

selected at regular intervals along the cat genome (Murphy

et al. 2007; Menotti-Raymond et al. 2009). Ninety-six

microsatellites were genotyped in the 2 pedigrees before

signiﬁcant linkage was detected with microsatellite FCA955

(LOD 5 2.79, h 5 0.2) on cat chromosome D2. Fine-scale

mapping was performed utilizing 7 previously published

microsatellite markers in the vicinity of FCA955 and 11

additional microsatellite markers selected from the in-

teractive cat genome browser GARFIELD ( http://

lgd.abcc.ncifcrf.gov/cgi-bin/gbrowse/cat) (Pontius and

O’Brien 2007) ( Supplementary material, Appendix 1). A

candidate region for SILVER was deﬁned as a 3.3-Mb

region, between markers FCA1240 (95.87 Mb) and

D2_99.21 (99.21 Mb) on chromosome D2 (peak LOD 5

10.5, h 5 0) (Table 1), which displays conserved synteny

to a genomic interval between 118.58 and 121.85 Mb on

chromosome 10 in the human genome. According to the

human genome (build 36), ( http://www.ncbi.nlm.nih.gov/

projects/mapview/stats/BuildStats.cgi?taxid 5 9606&build 5

36&ver 5 3) , this region includes approximately 17 genes

( Supplementary material , Appendix 2), none that have been

previously associated in other species with silver, dilute, or

hypopigmentation.

An attractive candidate gene in the feline SILVER interval

is SLC18A2, a member of the solute carrier family 18.

SLC18A2 has been described in humans and rodent models as

a vesicular monoamine transporter that accumulates cytosolic

monoamines into vesicles (Peter et al. 1995). Mutations in

related genes (SLC45A and SLC36A1) are responsible for

cream and champagne coat color hypopigmentation in horses

(Mariat et al. 2003; Cook et al. 2008), hypopigmentation in the

mouse underwhite (uw) phenotype (Lehman et al. 2000), and

pale skin in European populations (Lamason et al. 2005).

Analysis of the feline SLC18A2 is currently in progress.

We have thus mapped the SILVER locus in the domestic

cat, identifying a new genomic location for silver or

hypopigmentation in mammals. The absence of the pheome-

lanic agouti band in silver cats and the unique quality of orange

pigmentation in an orange, silver cat additionally suggests that

SILVER in the domestic cat may possibly play a role in the

elusive pheomelanic pathway—either in regulation of

synthesis of pheomelanin or in the structure or molecular

composition of the pheomelanic pigment.

Little is known about the regulation of the pheomelanic

pathway or about the structure, molecular composition, and

photobiology of pheomelanin (Simon 2003). The mapping of

a novel locus for SILVER to a relatively short interval offers

much promise in identifying a gene that may help elucidate

aspects of the pheomelanic pathway and illustrates the promise

of the cat genome project in increasing our understanding of

basic biological processes of general relevance for mammals.

Supplementary Material

Supplementary material can be found at http://www.jhered.

oxfordjournals.org/ .

Menotti-Raymond et al. Domestic Cat Mapping of the SILVER Locus

Funding

National Cancer Institute; National Institutes of Health

(N01-CO-12400).

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We thank Audrey Law for access to the male Egyptian Mau cat that was

used as founder of Pedigree One. Additionally, we thank Dr Lyn Colenda

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maintaining the silver pedigree. David Wells, Melissa Musser, and Adam

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does not necessarily reﬂect the views or policies of the Department of

Health and Human Services nor does mention of trade names, commercial

products, or organizations imply endorsement by the US Government.

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