Working With Autosomal Genes for Color
and Pattern: A Domestic Guppy Breeders
best friend and often worst nightmare…
Presented Sept.
5, 2015 to attendees of the 18th
World Guppy Contest held in Tampa, Florida, USA
© Alan S. Bias
Permission granted for nonprofit reproduction or
duplication of photos and text with proper credit for learning purposes only.
Abstract. The selection for genes
in Domestic Guppies has long been heavily based on sex-linked genes. In particular Y-linked for pattern and X-linked
for color. Over the last several decades
a larger percentage of strains and phenotypes (especially those created by Asian and European breeders) have been
produced based on autosomal genes or co-expression of sex-linked and autosomal genes.
The attempt of this presentation is to
help breeders gain not only an understanding of autosomal genes, but their
interactions in combination(s) and with other genes. The development of domestic genes, unlike
wild counterparts subject to predation, is only hindered by breeder selection
and retention. Results based on 45 years
breeding experience of which nearly thirty (30) years have been devoted to
strains collectively known as “Swordtail Guppies”, efforts of other professional
breeders, and that of the scientific community are presented.
Key Words: Guppy, Domestic Strains, Autosomal Genes, Autosomal Recessive, Autosomal
Incompletely Dominant, Wild-type, Breeder, Guppy Color and Pattern, Poecilia reticulata.
Introduction
Welcome to each and every one of
you. I’d like to thank you all for
taking the time and effort to attend not only the 18th World Guppy Contest, but
also this presentation. Your support as
Domestic Guppy breeders has ensured the success of this venue and its place in
GuppyC history and the memories of
those in attendance. Some of you I have
known for many years, others I have corresponded with for just as many years,
and others are of new acquaintance…
In
today’s presentation we will only be dealing with hereditable genes impacting
color and pattern. Not those dealing
with finnage propagation or others related to fecundity.
Discussion
Much
variation is found in wild guppy
colors & patterns as a result of habitat type (upper or lower stream setting), sexual selection, and
predation. Yet, only a singular “grey”
body color is found in wild guppies, often referred to as “wild-type or grey wild-type”. Domestic GuppyA
foundation stocks in the early 1900’s all derived from limited importations of
such fish. While unexpressed, the majority of all of the diversity
in modern phenotypes was contained in these initial imports or subsequent
collections that may have contributed additional mutations.
A large portion of the past
effort of both breeders and researchers from 1920 onward has focused on the use
and documentation of “sex-linked” traits found within genotypes to produce and
improve upon domestic phenotypes. While early research linked specific
expressions to individual “genes”, we now find that many are the result of
“multiple genes” or “gene interactions”.
As a pedigree breeder and part-time researcher I find it best if we refrain
from the use of the term “gene(s)” and instead defer to the use of “trait” in
discussions if you don’t have genetic evidence supporting how the gene is
inherited.
Sex-link genes can be identified,
and passed on by either the X or the Y chromosomes, or by both of them. Depending upon just how closely they reside
to the SRY; sex determining region of the Y chromosome, they may cross over
frequently from X to Y or Y to X, they may cross over rarely, or not at
all. In many instances crossover is
often overlooked in breeder tanks for a simple reason. That being “does the gene express in males only,
or both males and females?”
I’d like to take the opportunity
to focus on a singular mode of inheritance available within our genetic
“toolbox”; autosomal genes. Prior to
1930 only a single autosomal gene had been identified for color or pattern in Guppy
stocks; Zebrinus (Winge 1927). Autosomal
refers to genes located on any chromosome other
than a sex chromosome. In theory,
autosomal genes should affect the body color of both sexes equally. However, in practice this is not always the
case as specific genes may impact color expression limited to males (known as sex-limited genes). Zebrinus is an obvious example of a
sex-limited gene that produces a phenotype in only one sex. Females do not express any barred pattern.
Autosomal genes can be passed by
either sex in several modes of inheritance.
1.
Autosomal
Incompletely dominant,
2.
Autosomal
Recessive,
3.
Autosomal
completely dominant.
Initially,
basic identification of traits found in Guppy genotype was the product of
scientific research and publication.
While often lacking in formal documentation, identification of new traits,
or at least assemblage of complex phenotypes, has been the product of the
breeder community. Where
we often fail as breeders is in keeping complete records needed to document our
results. This results in much
speculation and inaccurate “facts” when disseminating our results among fellow
breeders.
Male sex-limited genes require
the presence of testosterone for expression.
Autosomal genes are passed to male and female offspring, and are expressed
in females. The
exception would be autosomal sex-limited genes, such as Zebrinus, which also
require male hormones for expression. When
a gene does not visibly express in females, X-linkage is easily confused with an
autosomal dominant gene. Dominance in
itself can be established for a particular gene with the first generation of reciprocal
crosses. Though this does not
distinguish between sex-linkage and an autosomal mode of inheritance. After an initial cross and expression, it requires
one or two generations of a reciprocal cross to distinguish between X-link dominant
and autosomal dominant.
Chromatophores are responsible
for projection of color and pattern in Guppies (See below: Figure I – Kottler
2013). Generally, five (5) types are
acknowledged; black melanophores, orange to yellow xanthophores, red
erythrophores, blue/green/silver reflective iridophores and white leucophores. Blue chromatophores (cyanophores) are present in some species and possibly Guppies(?). The autosomal genes we will discuss have
impacts on each of these classes.
Grey – Wildtype. There is no notation for a “grey gene” (See: Table I). The grey color in guppies is primarily due to corolla and dendritic
black melanophores. Generally, dendritic
melanophores are resident along upper and lower layers of scales. Corolla melanophores are found at lower levels of skin and
scattered around the body. Together they
produce the reticulated effect Guppies are named for: Poecilia reticulata. Few true mutations have been documented in Guppy research or identified by
Domestic Breeders. For the most part we
are simply identifying and working with genes.
Table I.
B – not blond
|
G – not golden
|
A – not albino
|
b – blond
|
g – golden
|
a – albino
|
[Note:
If a phenotypical expression is not blond, golden, or albino, it is
grey.
This list can be
expanded to include additional autosomal traits, the same principle applies.]
When combining genes
into a phenotype, the question then becomes are the various genes alleles of a
single gene or are they two or more entirely different genes? If two or more
genes are involved, are they located on the same chromosome or on different
chromosomes? If they are on the same chromosome, are they close enough to each
other that they tend to stay together during meiosis (cell division that produces gametes) or do the separate from each
other randomly?
When you view results of Grey
breeding's that are heterozygous for Albino (Aa), Blond (Bb), and Golden (Gg)
the overall intensity of both color pigment and melanophores (See: Table II.) are reduced through epistasis. We are dealing with three pairs of different
genes. Epistasis refers to the situation where one gene (or allele of that gene) modifies or inhibits the expression of a
different gene, gene pair, or an allele of the second gene (See: Table III).
Melanophore Size
& Structure Grey, Blond, Golden, and Cream (left – right) (Goodrich et. al
1944).
Table III.
bb is epistatic to G and A
|
gg is epistatic to B and A
|
aa is epistatic to B, G, bb and gg
|
bb
gg is cream
|
Eb
bb or Ab bb white
|
Eb
gg or Ab gg are silver
|
Two genes are alleles of each
other if they are alternate forms of the same gene. In example: the coat color series in cats is full color
(C), Burmese (cB), Siamese (cS), blue-eyed albino (cb),
and pink-eyed albino (ca). DNA sequencing has confirmed earlier
crossing data indicating each trait (phenotypical
expression) is due to different alleles (alternate forms of the same gene).
When two pairs of genes are
linked, they are located on the same chromosome and are close enough in
proximity to each other to avoid random recombination. They recombine at a frequency that is less
than 50%. Thus, if the genes A and B are linked, we may find four
different possible combinations of A
and B on a single chromosome: AB, Ab, aB and ab.
Grey Vienna
Emerald DS male & female, photo Alan S. Bias
Grey Wild-Type
male, photo courtesy of Ramona Osche Grey
Wild-Type female, photo Alan S. Bias
Autosomal
Genes For Color and Pattern
Albino
Lutino (l ). Recessive. Also known as Wine Red Eye Albino (WREA) or (Type
A). Eyes are a dark “Burgundy”
color. When photographed from a certain
angles will appear black. Likely
tyrosinase positive; enzyme present, with reduced melanin production. Lutino
(l) is allelic to
Grey (L, not-lutino).
Lutino Schimmelpennig
Platinum Snakeskin Roundtail, photo courtesy Denise Barbe’
Albino
(a). Recessive.
Also known as Real Red Eye Albino (RREA) or (Type B). Inability to
produce black melanophores in body and finnage.
In effects eliminates all classes of melanophores; dendritic, corolla
and punctate. Likely tyrosinase
deficient; inability to convert tyrosine into melanin. Albino is epistatic to both Blond and Golden genes;
thus mutant alleles of each may be found in the albino genotype (e.g., aa Bb, aa bb, etc.). Described:
Haskins & Haskins 19486.
Albino Full Red Delta, photo courtesy of Paulo Henrique Keijock Muniz Albino Yellow Vienna LS, photo Alan S. Bias
Albino
(?? ). Recessive. Also known as “Type C - Singapore”. Likely tyrosinase positive; enzyme present,
with reduced melanin production. Little
is known of this allele. It is likely
present, but confused with Lutino. [Note:
No photo available].
Asian
Blau (Ab); also (r2)
Europe and (Rr) Asia. Incompletely
Dominant. In heterozygous fashion red
color pigment is removed, but yellow color pigment and Metal Gold (Mg) is
little affected. This produces an
iridophore based phenotype. Snakeskin
patterns degrade in both heterozygous and homozygous expression. The Purple (Violet) sheen found above the
lateral line of both males and females is removed. In homozygous condition certain black
melanophores are removed along with red and yellow color pigments. In homozygous condition finnage is also
reduced in expression, but genes are still present in genotype for normal finnage. Outcross of homozygous Ab will produce
expected finnage in F1 offspring.
[Note: As there are distinct
types of red color pigment present in both body and finnage, removal may not be
complete in a red “Old Fashioned” shoulder stripe. A very faint “red shoulder stripe” is
sometimes visible.]
Heterozygous
Asian Blau Vienna Lowersword, photo Alan S. Bias
Homozygous Asian Blau Vienna Lowerswords, photos Alan S. Bias
Bar
(bar). Recessive.
Officially the pattern is described as being comprised of 3-5, or more,
dark vertical bands. Personally, I view
the pattern as being iridophore based stripes with “gaps” populated by
melanophores as a result of the interaction of iridophores and melanophores. If otherwise, the Bar pattern would
disintegrate in albino or blond form. Similar
in expression to sex-link Tigrinus, which is comprised of strait and forked
bands. Described: Phang
199913. (Note: See Zebrinus gene. Zebrinus and Bar while similar have
noticeable differences in expression.
Bar tends to solely express in vertical stripes, while Ze can express
forking on top of stripes).
Barred Snakeskin
Delta, photo courtesy V. Phang (1999)
Blond
(b). Recessive.
Also known as IFGA Gold, Asian Gold, European Blond. This mutation produces a near normal amount
of black melanophores of all types; Dendritic, Corolla and Punctate. However,
the size of each is greatly reduced and the structure modified as compared to
“wild-type” grey. According to published
results Blond is not linked to Golden. However,
results were based on limited numbers and interpretation. Results of breeders are often suggestive of
partial linkage. This gene should be
viewed not as a suppressor of melanophores, but rather one that alters size. Described:
Goodrich et al. 19444.
Blond Vienna
Lowerswords, photos Alan S. Bias
European
Blau (r or r1); also
(eb). Recessive. Also known as Dunkel in Asia. European Blau is not epistatic to wild-type
grey. It is epistatic to genes for red
and yellow; major red and yellow color pigments are removed from the body in homozygous
expression. Certain red color pigments may be present in finnage, and to a
lesser degree in body. Though reflective
qualities are reduced. Ecotopic
melanophores may be removed, while basal
level melanophores such as found in Half Black (NiII) are only slightly
reduced. Snakeskin patterns degrade in
homozygous expression. Purple (Violet) sheen found above the lateral
line of both males and females is removed. There is minimal impact on finnage
reduction. Described: Dzwillo
19591. [Note: As there are distinct types of red color
pigment present in both body and finnage, removal is incomplete in a red “Old
Fashioned” shoulder stripe. A reduced
“red shoulder stripe” remains visible.]
European Blau Grey Wild-Type, photo courtesy of Tobias Bernsee
Glass
Belly (gb). Recessive. In homozygous fashion removes / reduces
formation of both iridophores and leucophores over the entire body; including
peduncle, abdomen, gills and eyes. Producing
a clear/ translucent “matt finish” in areas expressing color pigment and Metal
Gold (Mg) or dark black in areas expressing black melanophores, such as the
eyes.
Glass Belly
Pingu, photo courtesy Carl Groenewegen
Golden (g).
Recessive. Also known as European Gold, IFGA Bronze or Asian Tiger. This gene produces a reduced amount of black
melanophores (50% +/-) of all types; dendritic,
corolla and punctate. However, the size
of dendritic and corolla melanophores are greatly increased and collection of
corolla is concentrated into "clumps" or "islands" of
melanophores along scale edges. Males
and females lack skin melanophores at birth, but develop with maturity. Scale edging will become lighter the higher
the inbreeding co-efficient; i.e. long-term Golden x Golden breeding’s.
According to published results
Golden is non-allelic and not linked to
Blond. However, results were based on
limited numbers and interpretation.
Results of breeders are often suggestive of partial linkage. This gene should be viewed as a suppressor of
melanophore population numbers. Described: Haskins & Druzba 19385 as
Fredlini (fr), Goodrich et al. 19444 as Golden
(g), and adopted by Haskins. [Note: In
Europe still often referred to as “Fredlini” in
regard to Golden stocks developed by Swedish Artist / Aquariust Tor Otto
Fredlin. This designation did not remain
in place as it described a guppy variantB;
Lebistes reticulatus (Peters) var. Fredlini
(Schreitm) instead of an allele of grey. Schreitmuller 193215, 193316, 193417.]
Golden Topswords,
photos courtesy Denise Barbe’
Hellblau
(r3). Recessive. Red
color pigment is entirely removed. Yellow
color pigment is almost completely removed, but Metal Gold (Mg) can be present. Unlike Asian Blau (Ab) or European Blau (Eb)
snakeskin pattern does not degrade. Any Purple
(Violet) sheen found above the
lateral line of both males and females remains expressed. As homozygous Hellblau fish mature reflective
qualities of iridophores overshadow early formed melanophores, producing an
appearance of “brightness”.
Hellblau
Snakeskin, photo courtesy of Gernot Kaden
Ivory
(I); Yoshiki
Tsutsui denoted as Violet (v). Incompletely Dominant. Ivory suppresses red color pigment. Resulting in a “white” appearance on modified
red fish and “violet” on modified blue fish.
According to Claus Osche, Ivory first appeared at TFI Farm in Singapore
in Red Mosiac (i.e. Blue Variegated), producing a “whitish- violet” coloration. According to Yuji Yamaguti, Japanese breeders
denote Purple Grass genotype as: Ivory
(ii) + Asian Blau (Rr). It is possibly
Purple Body Mutation (Pb) is also present. While Ivory is the product of a gene, Purple Grass
is a trait (phenotype) produced by
the action of ii Rr genes.
Ivory Grass, photo courtesy of Shinichi Kobayashi
Ivory Half Black, photo courtesy of Shinichi Kobayashi Ivory Galaxy, photo courtesy of Shinichi Kobayashi
Ivory Schim Plat. Delta, photo courtesy Akrawat Design Ivory Delta female, photo courtesy Harn Sheng Khor
Ivory Schim Plat. Delta, photo courtesy Akrawat Design Ivory Delta female, photo courtesy Harn Sheng Khor
Magenta
(M). Incompletely Dominant. Proliferation of red color pigment and
iridophores. This gene converts yellow
color pigment cells to red, though Metal Gold (Mg) may remain. Also, produces visible concentrations of
black melanophores in certain body regions.
Reduces fin development.
Magenta. Photo
courtesy of Krisztián Medveczki
Metal
Gold (Mg). Undescribed, likely Incompletely Dominant. Also
known as Material Gene in Asian and Metallic in Europe. Yellow-Gold iridophore gene. Comprises most body color found in Yellow
strains. Heterozygous expression not
visible in females, but visible in homozygous fashion. Heterozygous expression in males often
limited to portions of finnage and portions of body. Homozygous expression in males creates an
overall “metallic sheen”.
Homozygous Metal
Gold (Mg) Vienna Lowerswords, photos by Alan S. Bias
Hete. (left)
& Homo. (right) Metal Gold (Mg) IFGA Delta, photo courtesy of Bryan Chin
Metallicus
(Me). Recessive. Also
known as Stoerzbach (s) / Störzbach
Metal. Blue iridophore gene. Removal of red and yellow color pigments in
body, but not finnage. Individuals with
a Yellow-Gold cast result from addition of Metal Gold (Mg). Described:
Kempkes 20077.
Homozygous
Stoerzbach Grey (left) & Blond Metal Gold (right) Vienna Lowersword, photo
Alan S. Bias
Midnight
Black (mid). Recessive. Also known as Hypermelaninization. A form of “non-motile” black melanophores, is most commonly associated with Black Moscow strains. Expression of Midnight gene is visible in
females. Some breeders report expression
in F1 outcross of midnight females.
This is suggestive of Incompletely Dominant mode of inheritance.
Midnight Black Moscow, photo courtesy of Harn Sheng
Khor
Pink
(pk). Recessive.
Expression of standalone Pink in itself is easily overlooked in
wild-type. Pink is epistatic to the presence
of red color cells, resulting in removal in body and a “yellow-orange” cast in
finnage. Homozygous Pink has distinctive
impacts on various types of black melanophores; a reduction in co-expression
with NiII halfblack, an increase with Moscow Blau Additional Gene (MBAG) or
snakeskin genes. In the case of
reticulation an increase in concentration of melanophores is visible on scale
edging. Does Pink remove melanophores,
prevent their development, or convert the cells to a different cell class? Results seem dependent on co-expression with
other genes. In pkpk + NiII it appears
melanophores are removed or fail to migrate.
Yet, in pkpk + MBAG it appears melanophores are converted and proliferate. Pink can remove blue iridophores. This results in opaque body coloration or
white appearance in co-expression with Y-link Moscow (Mw) shoulder pattern. The most spectacular phenotypes are the
result of homozygous Pink co-expression with other full body or half body
melanophore and iridophore genes.
Homozygous Pink causes reduction in size and finnage. Each is retained in the genotype and restored
with an outcross.
Homozygous Pink
female, photo courtesy of Yuji Yamaguti
Homo. Pink, photo
courtesy of David Liebman Homo. Pink Vienna
Swordtails, photo courtesy Björn Lundmark
Saddleback
(Ht ). Autosomal Dominant. [Note: Some breeder reported results are suggestive
of an Autosomal Incompletely Dominant mode of inheritance, while others
strictly sex-linked. This suggests that there may be at least two and perhaps
three different genes with similar effects.] Also known as Half Tux. A black melanophore band runs horizontally on
the upper peduncle quadrant. This is normally
found in conjunction with corresponding yellow color pigment on lower peduncle
quadrant; this version is considered Y-linked.
Another version appears lacking corresponding yellow pigment on lower
peduncle quadrant; this version considered X-linked.
Saddleback
Roundtail, photo courtesy of Tobias Bernsee
Zebrinus
(Ze). Incompletely Dominant. Officially the pattern is described as being comprised
of 2-5, or more, dark vertical bands.
Personally, I view the pattern as being iridophore based with “gaps”
being populated by melanophores as a result of the interaction of iridophores
and melanophores. If otherwise, I would
expect the Zebrinus pattern to disintegrate in blond because their melanophores
are much smaller in size. But I would not expect the same with albino, because
the melanophore is still present with the same size as in grey, the albino
cells fail to synthesize melanin, but they are there. Similar in expression to sex-linked Tigrinus,
which is comprised of strait and forked vertical bands. Described:
Winge 192718. (Note: See
Bar gene. Zebrinus and Bar while similar
have noticeable differences in expression.
Bar tends to solely express in vertical stripes, while Ze can express
forking on top of forward stripes).
Grey & Blond Zebrinus Vienna Lowerswords, photos
by Alan S. Bias
Double Recessive Autosomal Genes
Cream. Double Recessive (Blond +
Golden). Crème is not due to a single
gene, it is a trait (phenotype)
produced by the action of two genes. In
females chromatophoes are not macroscopically visible. Melanophores
are reduced by >80-90%. Corolla &
Punctate body cells in Cream remain the same size as in blond. Dendritic cells on scale edges in Cream are
smaller than either Golden or Blond.
Cream not only greatly reduces the total number of black cells, but also
reduces remaining large dendritic cells in size. According to French breeder Denise Barbe’,
viability is reduced. Described: Goodrich
et al. 19444.
Double Recessive Blond + Golden (bbgg)
Coral Red Snakeskin, photo courtesy photo courtesy Denise Barbe’
Silver. Double Recessive (European Blau + Golden) or (Asian Blau + Golden). Silver is not due to a single gene, it is a
trait (phenotype) produced by the
action of two genes. Similar in appearance to White. Described by Hans Luckmann as having the
appearance of “tarnished silver”. Body
coloration is pale, though some pattern remains subject to limitations of
European or Asian Blau’s; removal of red and yellow color pigment. Finnage is flatter colored with limitations
of European or Asian Blau’s. Scales are
edged in black with a darker appearance.
Named by initial breeder Hans Luckmann who first combined and documented
European Blau + Golden.
European Blau (EbEb) + Golden (gg); i.e.
Silver, photo courtesy of Denise Barbe’ (left)
Half Black (NiII) Asian Blau (AbAb) +
Golden (gg); i.e. Silver female, photo courtesy of Tobias Bernsee (right)
European Blau (EbEb) + Golden (gg); i.e.
Silver, photos courtesy of Denis Barbe’ (left) & Stephen Elliot (right)
White. Double Recessive (European Blau + Blond).
White is not due to a single gene, it is a trait (phenotype) produced by the action of two genes. Melanophore size
and numbers are reduced. Body coloration
is pale, though some pattern remains subject to limitations of European Blau;
removal of red and yellow color pigment.
Finnage is flatter colored with limitations of European Blau. Described:
Dzwillo 19591.
White Half
Black Reds, photos courtesy of Tobias Bernsee
~~~~~~~~~~~~~~~~~~~~~~~~~~~
When Öjvind
Winge published The Location of Eighteen Genes in Lebistes Reticulatus in 1927 (Winge 192718)
he listed a total of 18 ornamental traits.
Seventeen (17) deriving from an X or Y sex-linked mode of inheritance,
and one as autosomal incompletely dominant;
Zebrinus (Ze). The foundation
male of this particular trait was obtained in 1918. As Zebrinus was the first identified autosmal trait for color or
pattern, he delayed publication for nearly eight years. In his words, “sex-linked inheritance with
frequent crossing-over between the X and the Y chromosome might easily be
confused with ordinary mendelian inheritance, and it was therefore desirable to
have an abundance of numerical material.”
While nearly 90
years have passed since the formal publication of Zebrinus as the first
documented autosomal gene for color or pattern, to my knowledge only an
additional six autosomal genes have been formally described; Blond (1938/1944),
Golden (1944), Albino (1947), European Blau (1959), Bar (1999), Metallicus [Stoerzbach]
(2007).
Researchers often use the term “accessory genes” to document unknown
grey areas. As breeders we have long
been aware of positive & negative “autosomal
enhancement”, or accessory genes through our improvements in color, pattern
and finnage through positive selection.
Control of gene expression of body
and finnage is generally considered to be separate and distinct. But this
distinction is not always written in stone.
This is easily seen in the distinct effects of European and Asian Blau
on finnage coloration (See prior photos). The use of "full body" genes can be
used to amplify expression of another trait, as seen with Asian Blau +
Schimmelpennig Platinum. This is formally referred to as “epistasis”.
Asian Blau + Schim. Plat DS, photo
Alan S. Bias
As a breeder I have observed autosomal
genes have direct impact on expression in both heterozygous and homozygous
states. Breeders have long been aware of this, though
may not have understood the implications.
This is most easily seen in “incompletely dominant” genes such as Asian
Blau (See prior photos). Asian Blau produces vastly distinct
phenotypes in either homozygous or heterozygous condition.
What most breeders often fail to
realize is “recessives” also have an impact on expression in heterozygous
condition. This expression is often very
subtle, and you must understand not only your strain genetics, but that of each
line. The degree of expression of the “recessive”
allele in the heterozygote may vary from strain to strain because of the
genetic background of the particular strain. This has occasionally been documented in other
species. A good example to cite involves Red or Yellow strains, either solid or
halfblack (NiII), with lines maintained in Grey (BB) and Blond (bb). Both red and yellow have documented associations
with melanophores; when either color pigment is present, so are melanophores. Each type of color pigment has epistatic
“repulsion” qualities that determine not only not only melanophore locations,
but also concentration levels. Normally,
melanophores will populate regions absent of color pigment or be forced to
extreme edges.
It is common practice for breeders
to maintain dedicated Grey (BB) and Blond (bb) breeding lines within a
strain. Often the Grey line is
maintained in homozygous condition. In
my breeding program I routinely maintain my Grey lines in heterozygous Grey (Bb) condition. This means a percentage of males are also homozygous
for both Grey (BB) or Blond (bb). This
allows me to select Blond males for use in outcross to dedicated Blond breeding
lines, and avoid heterozygous grey-bodied (Bb) males in F1
offspring.
When lines of grey fish are bred
long-term grey x grey in homozygous (BB) condition the intensity of coloration
increases, along with the concentration and size of melanophores. In time they become “dirty” from the excess
accumulation of melanophores. In turn breeders
routinely outcross them to Blond (bb) counterparts. Resultant F1 grey bodied
offspring, which are heterozygous (Bb) for blond, receive direct benefit both from
the Blond gene and outcross.
1. Blond
reduces melanophore size in both homozygous and heterozygous fashion.
2. Out
crossing reintroduces the dominant allele(s) of the modifier gene(s) and
returns the F1 (or beyond) to the more desired condition. Inbreeding
led to homozygosity for modifer genes (QTLs) that caused a “dirty” appearance.
When Blond (bb) fish are bred
long-term bb x bb the intensity of coloration decreases, along with the
concentration and size of melanophores.
In time they become “pale” from the excess reduction of
melanophores. In turn breeders routinely
outcross them to heterozygous (Bb) or homozygous (BB) grey counterparts. Resultant F1 offspring, receive
direct benefit from outcross. Again, outcrossing
reintroduces the dominant allele(s) of the modifier gene(s) and returns the F1
(or beyond) to the more desired condition. Inbreeding led to homozygosity for
modifer genes (QTLs) that caused a “pale” appearance.
I have found when grey fish are bred
long-term for heterozygous (Bb) condition (Bb x bb or Bb x Bb) there are noticeable differences in the intensity
of coloration, along with the concentration and size of melanophores. Homozygous grey-bodied male siblings express
more intensity of coloration, the same as found in dedicated Grey lines. Heterozygous grey-bodied males lack the same
intensity of coloration as found in homozygous grey-bodied male siblings. As outcross is not a factor, this is highly suggestive
of direct influence from the autosomal recessive Blond gene when in
heterozygous condition. These recessive
genes are not completely recessive, but so close to being recessive that it
requires careful examination to detect the heterozygotes. [Note:
This observation is not limited to
autosomal gene Blond. I see the same correlation
in other autosomal recessives in heterozygous condition; Golden (Gg),
Stoerzbach (Ss), Albino (Aa), and Pink (PKpk).]
To illustrate the effect of
heterozygous Blond on Grey wild-type (see
below), we show a Grey (Bb) male heterozygous for Blond photographed under
three lightings. Notice muted Wingean
Orange spots and minimal black ocular spotting in anterior shoulders and
finnage. This degree of spotting is
commonly found in grey bodied males in my Lowersword strain. While he expresses a fairly high degree of
iridescence, overall color pigment expression is minimal and melanophores
reduced. [Note: Variegation (Var) is visible in dorsal and
caudal, but faintly expressed.]
In comparison we have two homozygous
Grey (BB) males (see below) with a
high degree of iridescence and reflective qualities in color pigment. The male on the left in Purple Body Mutation
(Pb), and the male on the right in wild-type orange.
Heterozygous Grey male (Bb), photos (left
– right) Alan S. Bias, photo (lower) courtesy of Joe Mason
Homozygous Grey (BB) males, photo by
Alan S. Bias
In the following 2 examples we
illustrate the effect of heterozygous Golden (Gg) on Grey (bb) wild-type (see below). No additional Y-linked genes for fragmentary
snakeskin have been introduced. The
Golden gene was infused into my stocks several years ago through a single homozygous
Golden (gg) female. Notice how
melanophore collection and locations are altered from the prior examples
above. This is the “expected norm” for
heterozygous (Gg) breeding’s in my stocks.
Thus, is highly suggestive of direct influence from the autosomal
recessive Golden gene when in heterozygous condition.
Heterozygous Golden (Gg) males,
photo by Alan S. Bias
Summary
& Conclusion
When taken seriously, Domestic
Guppy breeding may not be Rocket Science, but it is a science within itself as
is any form of pedigree stock breeding. Longtime successful stock breeders breed by eye; through the power
of observation to achieve if not understand results. We are visual
thinkers to varying degrees. Successful breeders
have an inherent and often above average ability to observe
the natural world and create domestic results (Arnheim 196919, Grasseni 20042, 20053). Yet few take the time to
learn the applied genetics needed understand both past, present and future
results of planned breeding’s.
The
Poecilia reticulata genotype is contained in a diploid chromosomal set of 46
chromosomes found in pairs, 44 of which are autosomal and 2 sex determining. Nearly all of the genes for color and
pattern are identified as sex-linked. In
a loose sense, assuming equal chromosome sizes, this equates to color and
pattern genes being located on 4% of the total genome, leaving for us as
breeders 96% of the total genome to search for unknown autosomal modifiers of
color and pattern to hide.
No new color is being added to
our genetic toolbox as breeders.
Genotype has been fixed since the inception of Domestic Guppy Breeding
by the five identified types of chromatophores that determine color and
pattern. Or has it? Much new color and pattern has been added to
phenotypical expressions in recent decades.
Some of which results from the identification of autosomal modifiers
found in existing stocks. However, the
greatest potential source of new color genes and gene combinations is wild
populations, as evidenced by the incredible color traits being developed from
infusion of variant populations.
The
implications should be readily visible to any long-term breeder. We still have a vast unknown in the Guppy
genome to explore in our search for additional autosomal genes. Modifiers which can be used to further create
new and diverse autosomal combinations with existing sex-linked genes.
Regardless
of your interests as a breeder; production to set show standards, creation,
exploration or an overlapping interest of all.
Don’t be so quick to cull that anomaly that shows up. Keep some notes or take a digital photograph
to record. More importantly, pass it on
to a breeder who may have the interest to study and develop it.
Just because a class does not
exist to exhibit results today, does not mean it will not exist in the future.
Just because a new expression
does not meet a standard of today, does not mean it cannot be improved upon in
the future.
I sincerely thank you all for
taking the time to attend this presentation today…
DEFINITIONS
Alleles: Alternate
forms of the same gene.
Domestication:
To bring or keep
(wild animals or plants) under control or cultivation. http://dictionary.reference.com
Dominance:
One gene contributes more, or
less, to the final phenotype. In complete dominance one allele completely hides
the effect of the other allele; while in the case of incomplete dominance, the
phenotype is part way between the phenotype of the two homozygous forms of the
allele.
Heterozygosity: If two different alleles for a specific gene are present.
Homozygosity: When an allele inherited from
a sire is the same as the one inherited from the dam.
Inbreeding
Depression: A reduction
in fitness due to the mating of closely related and often genetically similar
individuals; creating a loss of robustness due to expression of deleterious
recessive alleles. This may result in an
inability to respond to selection from lack of residual heterozygosity.
Inbreeding: The mating of highly related individuals
such as father to daughter or brother to sister. An inbred individual or population often
shows increased homozygosity. Progeny
may exhibit a reduction in desired genes or loss of fitness.
Linebreeding:
Planned mating to maintain a high degree of relation to a common ancestor or
ancestral group of high regard. The
intent is to avoid a reduction in desired genes or loss of fitness. A linebred individual has at least one common
ancestor on the sire and dam side within 3-5 generations.
Meiosis: A type of cell division which reduces
chromosome numbers by half. Two successive
nuclear divisions occur, Meiosis I (Reduction - ploidy level from 2n to n) and
Meiosis II (Division - divides the remaining set of chromosomes). Meiosis
produces 4 haploid cells, while Mitosis produces 2 diploid cells.
Mutation: A mutation is a permanent change in the DNA sequence of a gene.
Mutations in a gene's DNA sequence can alter the amino acid sequence of the
protein encoded by the gene. http://learn.genetics.utah.edu/archive/mutations
Nonadditive
Gene Interaction: Non-additive
gene interactions include the effects of dominance of one allele over
another and epistatic effects of one
gene (or gene pair) on another, non-allelic gene (or gene pair).
Outcrossing:
The mating of unrelated or distantly related individuals. This
results in increased heterozygosity.
QTL: Quantitative Trait Loci – Section of DNA (the locus)
correlating to variation in a phenotype.
Statistical analysis is then used identify linkages with genes
controlling phenotype.
Acknowledgments
Richard Squire, Ph. D.
(Genetics), Retired Full Professor of Biology, University of Puerto Rico,
Mayaguez Campus. For his suggestions,
technical edits and proof reading of this publication.
Carl Groenewegen, Guppy Gene
Collector & Breeder, Liberty Twnshp., Ohio, USA
For his insights as a breeder, edits
and creation of a supporting PowerPoint presentation.
Claus Osche, Guppy Breeder &
Gene Researcher, Altenburg, Thuringia, Germany
For his insights as a breeder.
Yuji Yamaguti, Guppy Breeder
& Gene Researcher, São Paulo, Brazil
For his insights as a breeder.
Notes
A: The term “Domestic Guppy” in this article shall
collectively refer to any and all captive bred strains, regardless of genetic
inputs from variant populations of P. reticulata, P. reticulata
(wingei), P. reticulata (obscura).
B:
The terms “Variant
Populations” or “Variant” in this article shall collectively refer to any and all
described species of Guppy; P.
reticulata, P. reticulata (wingei), P. reticulata (obscura), P. reticulata
(guppii).
C: The term “Guppy”
in this article shall collectively refer to any and all captive bred or wild-type
populations of P. reticulata, P. reticulata (wingei), P.
reticulata (obscura).
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