Polymorphism and Gene Interactions
The existence of more than one form of a particular phenotypic trait in a population
is known as polymorphism. Polymorphism can derive from
- multiple alleles at a single gene locus
- interactions among multiple gene loci
- interactions among multiple gene loci, each with multiple alleles
- environmental influence on gene expression
monogenic trait - a single phenotypic trait whose expression is controlled by the action of a single gene locus.
polygenic trait - a single phenotypic trait
whose expression is controlled/affected by the action of more than one gene locus.
Monogenic Trait Variability: Multiple Alleles at a Single Gene Locus
Many genes have more than two alleles,
and not all the alleles have equal dominance/recessiveness. While this is not, strictly speaking, a case of gene interactions, it can account for a range of phenotypes that can resemble the results of gene interactions. (At the molecular level, there are very likely multiple genes contributing to these phenotypes.
Different combinations of multiple alleles at a single locus can produce a range of phenotypes.
For example, white variegation (V) "chevron" pattern in
Clover (Trifolium sp.).
Coat color in many mammals is affected by the activity of the agouti gene (A). In rabbits and rodents, mutant forms of the agouti gene result in different colors.
The agouti gene is not directly responsible for producing these patterns. It is very likely a master switch gene that regulates the activity of multiple genes, and is involved in multiple metabolic functions. Some of them surprising.
Discovering the function of master switch genes can help us understand metabolic disorders that can then be investigated for genetic treatment.
Codominance vs. Incomplete Dominance
The alleles of a single gene can interact in ways that result in
phenotypic ratios in offspring that are not predicted by Mendel's Laws.
Two such phenomena, not to be confused with one another are
Two alleles both produce proteins, but one is
non-functional. This results in heterozygotes producing only half
the amount of protein produced by a homozygous dominant individual.
Two alleles of the same gene are expressed, and
both products are functional, though different.
Examples of Incomplete Dominance
Flower Petal Color in Japanese Four o' Clocks
in the Japanese Four o' Clock, Mirabilis
There are two alleles of a gene for flower petal red
The wild type R1 allele codes for an enzyme vital
for the conversion of the precursor in the flower into the xanthophyll
- R1: red pigment produced
- R2: no pigment produced
- R1R1: red petals
- R2R2: white flowers
- R1R2: pink flowers
The mutant R2 allele produces an enzyme incapable
of catalyzing the reaction.
This recalls the importance of Inborn Errors of Metabolism:
- normal (wild type) allele - functional enzyme
- mutant allele - nonfunctional enzyme
Tay Sachs Disease
A defective allele, found most often in populations of Ashkenazi Jews (Eastern
Europe), results in a wild type enzyme (hexosaminidase-A) being produced
in a non-functional form.
hexosaminidase-A is responsible for breaking down lipids.
In its absence, sphingolipids accumulate in the developing brain and peripheral
nervous system of affected fetuses/young children
Result: brain damage, mental impairment, death by age five.
- TT: normal
- Tt: half the amount of enzyme produced, but sufficient
for normal development
- tt: no functional enzyme; expression of Tay Sachs
- This is Incomplete Dominance because both alleles are expressed (i.e.,
a protein is made from each allele), but only one is functional.
Examples of Codominance
Human ABo blood groups
Humans with type
AB blood have two different immunoglobins (IA and IB)
inserted into the blood cell membrane. Types A or B have either
one or the other, and type o has neither.
Note: The A & B alleles operate by modifying
a wild type mucopolysaccharide terminal sugars.
Note that Sickle Cell Anemia is
another case of codominance; Two different types of hemoglobin are
produced in the heterozygote, though the wild type ("normal") hemoglobin
provides normal functionality.
type A individuals have a modified enzyme (alpha-3-N-acetyl-D-galactosaminyl
transferase), which modifies the terminal sugars like so:
type B individuals produce alpha-3-D galactosyl tranferase, which modifies
the terminal sugars of the "o" type like so::
Polygenic Traits: Forms of Interaction
When multiple genes affect a single trait, their effects can be additive, or one gene can interfere with the expression of another gene at a different locus. In this section, we'll explore some of the various ways different gene loci can interact to affect phenotype.
When a single gene affects the expression of more than one
phenotypic character, the phenomenon is known as pleiotropy (from the Greek pleio meaning "more" and "trop, meaning "change").
Sickle Cell Anemia
The amino acid tyrosine is the precursor for (among other things), both forms of the vertebrate pigment melanin.
A mutation that results in a non-functional enzyme anywhere along the pathway will cause a failure to produce one or both forms of melanin.
The result affects the expression of multiple phenotypic characters
- eye color
- skin color
- hair color.
- sensitivity to sunlight
- vision (melanin is necessary for normal eye development)
The mutation which changes the 6th amino acid from the terminal end of the
Beta-protein chain is changed from glutamate to valine, making the chain
hydrophobic rather than hydrophilic. Because the mutant hemoglobin
precipitates readily in slightly acid conditions (as when the
sufferer undergoes physical exertion, dissolving CO2 in the blood), and the
malformed rbc's clog the capillaries, causing multiple characteristic phenotypic expressions:
as well as...
- malformed red blood cells
- slowed blood flow due to malformed rbc's
- "tower skull" phenotype due to hypertrophy of red marrow in the cranium
- stunted growth
Recall the silver lining: Heterozygote Advantage in areas where malaria is endemic.
Homozygous wild type people have a high incidence of
malaria, which can be fatal.
Homozygous recessive sickle cell individuals usually have shortened lifespan
due to the genetic disorder, but they are not susceptible to malaria.
Heterozygotes suffer few or no problematic symptoms of sickle cell anemia, nor are they susceptible to malaria.
An epistatic gene locus is one that affects the expression of alleles at another, separate gene locus. The gene locus whose expression is affected by the epistatic locus is said to be hypostatic. Multiple genes, each with more than one allele, can interact to produce unexpected phenotypes due to epistatic interactions.
Pleiotropy can be a result of various epistatic/hypostatic gene interactions, but there are many others, such as...
Comb Shape in Chickens Rose gene: R or r
Pea gene: P or p
Two loci, each with two alleles, interact to produce four possible phenotypes:
- Rose gene, if present in RR or Rr will produce a "rose type" comb--
but ONLY if Pea gene is present in pp condition.
- Pea gene, if present in PP or Pp will produce a "pea type" comb--
but ONLY if Rose gene is present in rr condition.
- If one dominant allele is present for BOTH pea and rose,
a "walnut type" comb results. R_P_ will give "walnut" comb.
- If both alleles are present in double recessive condition,
(rrpp), the wild type, single comb results.
Sometimes only a particular allele of an epistatic gene will mask the full
expression of alleles at a hypostatic locus.
If the allele of the epistatic gene happens to be recessive, the resulting interaction is known as recessive epistasis.
A simple example would be albinism.
Epistasis/Hypostasis alter Metabolic Pathways
Obviously, the genes themselves do not carve chicken combs out of tissue. Rather, the interacting genes can change a biochemical or
develomental sequence. Such gene actions are not always simultaneous, as not all genes "turn on" at the same time during embryo development.
For example, coat and skin color in Labrador Retrievers can be explained by the non-simultaneous action of two gene loci, B and E.
The B locus controls the color of melanin pigment: B is black; b is brown
The E locus prevents melanin from being fully deposited in the hair shaft: E is full pigment; e is diluted pigment
The E locus is epistatic to the B locus: It prevents the complete deposition of the (already-made) melanin pigment in the hair shaft, though it does not affect deposition in the skin.
Thus, the epistatic locus operates "developmentally downstream" (i.e., after the B locus is already expressed) from its hypostatic gene.
The golden coat is an example of recessive epistasis: the recessive allele of a gene (i.e., the e allele that prevents pigment deposition) exerts epistasis over another locus (the B locus, controlling pigment color), resulting in the pale-colored hair shafts.
- B- E- will be black (fur and skin)
- B- ee will be yellow fur, dark skin
- bb E- will be brown fur, brown skin
- bb ee will be yellow with brown skin
Gene Interactions Produce Polymorphism
There are countless polygenic traits, from the mundane to the unusual.
In any population (i.e., group of organisms of the same species that interbreed and live in the same place at the same time), the gene interactions that produce a range of phenotypes for a particular trait can sometimes be traced to the interaction of only a few gene loci.
Fruit color in Bell Peppers
At least three loci interact to produce a variety of fruit colors in these plants.
- Y - timing of chlorophyll elimination (Y - early; y - normal)
- R - color of carotenoid pigments (R - red; r - yellow)
- C - regulation of carotenoid deposition (C - normal; c1, c2 -
Different combinations of alleles at the three loci produce multiple phenotypes:
- Y- rr c1c2 - pale yellow
- Y- rr Cc2 - darker yellow
- yy rr CC - green
- Y- R- CC - red
- yy Rr CC - purple
- Y- Rr Cc2 - pale yellow
Skin color in Corn snakes (Elaphe guttata)
Vertebrates can manufacture two different forms of melanin, brown/black eumelanin and reddish brown phaeomelanin.
Mammal Coat Color
At least five genes interact to determine the coat color of mice, and similar genes govern coat color and pattern in other mammals. These vary across species, but their source is common ancestry.
The Agouti (A) locus - Determines the distribution of melanin in the hair shaft.
- wild type A = agouti
Various alleles exist that produce
- no yellow band (a)
- "black and tan" (at)
- yellow (AY)
...depending on their combinations and homo/heterozygosity.
The B locus - Pigment coloration. B = black; b = brown
The C locus - Expression of pigmentation C = normal color; c =
albino; ch = "Himalayan" (color sensitive)
The D locus - Controls amount of pigment in the hair shaft.
D = wild type; d =
dilute (The recessive allele is a modifier gene that affects the expression
of the other genes. It is epistatic over those other genes.)
The S locus - controls presence or absence of white patches
A closer look: Coat Color in Horses
color in horses is a complex affair, and some mutations are specific to certain breeds of horses. Murindu!
For those interested in current research in mammal coat genetics, check out the Barsh Lab at Stanford University.
Discovering the Nature and Mechanisms of Gene Interactions
Mendel had no tools for discovering how genes interacted. Later researchers devised ingenious experimental methods for generating mutants and observing the effects in the mutants' phenotypes, and how mutant traits were passed to subsequent generations.
Genetic Dissection via Analysis of Mutants
- Mutational analysis is the process of analyzing the phenotypes of
organisms known to be mutant for a particular wild type allele.
- The genetic field of mutational dissection involves the
intentional disruption of wild type alleles in study organisms, and the
study of the effect of that mutation on the organism's phenotype.
- Phenotypes of interest can be generated by exposing study
organisms to known mutagens, and observing the resulting phenotypes.
(you never know, at the initial outset, what you might get.)
- If a particular genes locus is known, it can sometimes be
targeted and "knocked out" so that its function in a normal organism
can be studied.
- Gene function can also be studied by leaving the gene itself
intact, but disrupting the function of its mRNA transcripts, or even
its encoded protein product.
- Genes that eliminate or reduce the function of a wild type gene
product are known as loss-of-function mutations
- Genes that increase or change the activity or function of a gene
product are known as gain-of-function mutations
Complementation: Inferring Gene Interaction
In natural populations, the two alleles carried by most individuals result in
wild type phenotype. Mutations may occur
spontaneously, but rarely the same way in any two individuals.
This means that if a mutation occurs in a particular member of the
species, and it passes on that mutation to its offspring, then inbreeding
between those two related individuals is far more likely to result in
homozygosity of recessive, mutant alleles than outbreeding with unrelated
To study the contribution of various genes to a particular
trait or biological process in an organism, one must locate (and sometimes induce) mutations at the various loci involved in that trait's expression.
For example, if one wished to determine the contribution of various
genes to some mode of locomotion in a worm (undoubtedly a trait/process
affected by many genes), you need to find mutant worms who have abnormal
If you have worms with abnormal locomotion, you'd like to find which
of these mutant strains have changes at loci different from one another, each of which may affect locomotion in a different way.
This means that to develop your strains of interest, you must breed
them together to see whether the alleles they pass on will complement the
alleles of other mutant strains--or have no affect on the locomotion
problems you already see.
One way to do this (if your study organism happens to be easy to breed, at
least) is via a complementation test.
Petal color in Harebells
- Wild type Harebells have blue flowers (produced by anthocyanin pigments)
- In the lab, you irradiated the flowers --> mutant gametes
- By breeding your mutant's seedlings together, you got three
different true-breeding strains, X Y and Z
- Only recessive mutants will work in a complementation test
- So the first step is a back-cross to the wild type parent to get
F1 for each mutant strain.
- F2 for each strain gives typical Mendelian ratios
- But where are the mutations? Are they all in one gene? Or more
than one? You can tell by doing complementation matings.
- Let's have a look at the mutant HareBell flowers
- turns out that in our made-up example, there are two genes, each
of which codes for an enzyme in the anthocyanin pathway.
Inborn Errors of Metabolism: When Genes Go Bad
The field of Biochemical Genetics is devoted to the study of genetic
control of biochemical pathways.
Many human disorders are known to be inborn and due to flaws in the enzymes
that convert one cellular substance into
For example, an error in any number of enzymes in the phenylalanine
pathway can result in a several different types of disorders
The amino acid (abbreviated "aa") phenylalanine is a precursor to tyrosine, an aa that serves as a
precursor to many different celllular products.
- In a normal metabolism, phenylalanine is converted to tyrosine by an
enzyme phenylalanine hydroxylase (p.h.)
- A mutant form of p.h. is unable to change phe to tyr.
- In humans
with this faulty enzyme, phe eventually breaks down into toxic, lipophilic waste
products (phenylpyruvate) that deposit in the nervous tissue and damage the CNS.
severe mental retardation due to phenylketonuria.
But there's a happy sidelight to this discovery...
In utero, the mutant fetus gets enzyme A from mom. Toxic buildup
of waste does not happen until after birth.
In the 1950's, it was discovered that PKU kids put on a diet low in phe
did not develop phenylketonuria.
By about age 6, the sensitive period has passed, and normal diet can
resume without damage to the CNS.
Today, about 90% of infants are tested for PKU at birth.
New problem! If a homozygous recessive PKU woman becomes pregnant, the high levels of
phe breakdown products in her blood can cross the placenta and damage the
CNS of her unborn child, even if the child is heterozygous and would not be
a PKU sufferer.
To prevent "maternal PKU", mom must resume her low phe diet during
pregnancy. It's not 100% successful, but it's better than nothing.
The mutant allele is most common in descendants of northern
Mutations in many enzymes in the tyrosine pathway can cause other inborn errors of metabolism.
a defect in any one of several enzymes in the series that changes tyrosine to
thyroxine results in a form of cretinism.
Alkaptonuria ("black urine disease") results from a defect in the
enzymatic pathway from tyrosine to harmless waste products (carbon dioxide
and water). Hydroxyphenylpyrivate breaks down into homogentisic acid, and
without the enzymes to break it down, it is excreted in the urine.
Interestingly, homogentisic acid turns black upon exposure to oxygen.
A defect anywhere in the enzymatic pathway from tyrosine to melanin (about 17
steps) can lead to albinism.
Cystic fibrosis is caused by a faulty protein that in wild type form
controls chloride ion transfer across cell membranes in secretory cells.
common mutation that causes this disorder can be seen HERE.
- The mutation shown results in deletion of
phenylalanine from a chloride-permeable channel membrane protein.
- Deletion of the phe disrupts normal chloride channel function.
resulting imbalance of chloride and sodium ions results in abnormally dehydrated
mucus which causes a multitude of physical problems, from sterility to
Many metabolic pathways involve the products of several genes that work together to facilitate a given process.
Enzyme function depends largely on the amino acids of which it is
composed, and their precise order. This, in turn, is controlled by the nucleotide sequence of the DNA encoding that particular protein.
Since the enzymes determine much of the rest of the organism (including
some of the construction of structural proteins and other cellular
products), a mistake in the DNA coding for an enzyme can have dire
consequences reflected in the physical and/or metabolic makeup of the
- active proteins (e.g. enzymes, microtubule proteins, membrane pump
proteins, antibodies) - these perform chemical functions
- structural proteins (e.g., silk, keratin, collagen) - these make up the physical structure of the organism
Archibald Garrod first wrote in 1909 that a number of human diseases were
probably caused by "Inborn Errors of Metabolism": some fault in a
metabolic pathway due to (almost always) deleterious mutation of a normal
wild type allele of a gene is the one that is most often
found in a natural population of a particular species.
mutant allele of a gene is the one that is changed (mutated)
from the wild type, and is found less frequently in a natural population.
- Most often (not always), wild type is encoded by a dominant allele
- It usually codes for a functional form of an enzyme
- Most often (not always), mutations result in a recessive allele
- It usually (not always!) codes for a non-functional form of
the wild type enzyme
The first scientists to study this phenomenon in detail were George
Beadle and Edward Tatum, who initially worked on an ascomycete fungus,
Neurospora, and later on Drosophila. By selecting mutants
known to have faulty enzymes in a given metabolic pathway (auxotrophs),
Beadle and Tatum were able to compare them to metabolically normal
organisms (prototrophs) to discover the enzymes mediating entire metabolic pathways.
They did this by using known auxotrophic Neurospora . As you will recall,
A prototroph is an organism that can survive and grow normally on
"minimal medium"--agar supplied with only the most basic ingredients for
survival (inorganic salts, a carbon source and water).
An auxotroph is a strain of that organism (bacteria or fungi, in most cases)
unable to survive on minimal medium without the addition of some nutrient
that it cannot make for itself (unlike a prototroph).
A leaky mutation reduces but does not destroy phenotypic expression of
A null mutation results in a completely non-functional version of the
wild type enzyme.
A silent mutation is a change in base sequence that does not alter
wild type enzyme function.
An information transfer mutation changes the way the mRNA transcript is
read. Such a mutation may do any number of things, including...
- alter the way introns and exons are excised and spliced
- change the promoter of a gene, resulting in altered gene expression.
- alter the nature (and stability of the header and/or leader of
the mRNA transcript.
Certain alleles, when present in homozygous
recessive condition, cause inviability/death of the homozygous individual.
By definition, the gene that has mutated is said to be an essential gene, since
its "demise" causes death of the organism that doesn't get its product.
This is an allele that reverses the effects of a recessive mutation
at another locus, causing the organism to revert to wild type phenotype.
But how? There are several ways...
nonsense suppressors - Sometimes a mutation will occur that causes
premature termination of protein translation (i.e., it inserts a STOP
(nonsense) codon in the middle of a protein transcript).
However, a tRNA anticodon mutation that allows a tRNA to attach to a stop codon
will allow continuation of the protein manufacture. The nonsense mutation is suppressed.
congruent protein mutations - If one protein suffers from a mutation
that changes its shape (and hence its activity with another protein), this
can be overcome if the protein "mate" also undergoes a mutation which makes
the two of them work together again.
modifier mutations are mutations in a gene that affects the degree of expression of a trait controlled by another locus. (An example is the "dove" or "cinnamon" coat colors of the gerbils we studied earlier, with "dove" being a modified black, and "cinnamon" being a modified agouti coat.) Which brings us to...
Penetrance and Expressivity
Environment plays an important role in gene expression.
In the genes we have studied so far, a mutation is expressed:
- if dominant, in either the homozygous or heterozygous condition
- if recessive, if homozygous
This is not always the case.
is the proportion of individuals with a specific genotype who
manifest that genotype at the phenotypic level. (Some individuals may not
express a gene if modifiers, epistatic genes or suppressors are also
present in the genome, which thwart expression.
Penetrance = 1.0 (100%) when all homozygous recessive individuals express
the recessive form of the allele, and all homozygous dominant individuals
and heterozygous individuals express the alternate form of the allele.
Penetrance < 1.0 if not all homozygous recessive individuals express the
Example: Brachydactyly in humans
Genetic Interactions and Pathology: Sickle Cell Anemia
Variable expressivity can often be explained by gene interactions.
is the degree to which a particular genotype is
expressed in the phenotype of a particular individual. (That is,
may be altered by heterogeneity of other genes which affect the expression
of the particular locus in question, or by environmental
Neurofibromatosis in humans causes tumorlike growths to appear
all over the surface of the body if it is fully expressed. In mildly expressed cases, the person with this genotype may never have anything more severe than a few cafe au lai spots on the skin.
Piebald spotting in beagles (and some other mammals): dogs who have the
same genotype for the piebald locus often express various patterns and
total coverage of white fur patches.
Essentially, penetrance describes what happens in a population, and
expressivity describes what happens in a particular individual.
Phenotype and Current Conditions
Human eye color is controlled both by several gene loci and the surrounding lighting.
Several loci contribute to the amount of melanin deposited in the stroma of the iris.
Eye color genetics is complex, but fun
- Very little melanin - blue
- Lots of melanin - dark brown
- And variations in between
Blue isn't a pigment. It's a result of structural refraction.
Here's some news for all you blue-eyed folks out there.
Internal Environment Can Affect Gene Expression
As an organism passes through its life cycle, the expression of its genes
changes. This means that some genes are not expressed until later in
Sex-Dependent Gene Expression
In sex-influenced traits, expression varies depending on the sex of the
carrying the alleles.
e.g. - finger length (we already did this one)
In other cases, autosomal genes cause the expression of a trait ONLY in
one sex or the other.
Example: Feathering morphology in chickens: h+h+ - hen feathering in either female or male
h+h - hen feathering in female; cock feathering in male
hh - hen feathering in female; cock feathering in male
h+ - hen-feathering in male or female (short, erect tail, short body plumage)
h - cock-feathering in male, if homozygous (long tail, long body plumage)
Females express hen feathering, no matter what their genotype.
Other examples of sex-limited traits: horns in some mammals
lactation in female mammals
ovaries in females; testes in males
various secondary sex characteristics
In some instances, an environmental factor can mimic the effect of a
mutation, if the factor is present during a critical point in
Presence of rubella virus during the first 12 weeks of pregnancy in humans
can mimic the phenotypic effects of certain rare, recessive alleles (at
several different loci) which can cause deafness, cataracts and defects in
Thalidomide (a drug administered in the 1950's to woman at risk of
miscarriage) mimicked a rare genetic mutation causing a disorder known as
phocomelia--failure of the long bones of the limbs to develop. (Note that
thalidomide did not produce a phenocopy effect in the test mammal,
The formation of birth defects due to environmental
agents (viruses, chemicals, etc.) is known as teratogenesis.
The impact of a gene at the
phenotypic level depends not only on its dominance/recessiveness, but also
on the modifying effects of other parts of the genome and on the internal
and external environment's impact on expression.
This brings us to the not-all-that-age-old question: Which is more
important in the formation of the organism, Nature (genotype) or Nurture
The answer may turn out to be....it depends.
The genotype may set the limits for a
particular organism's phenotypic potential. The environment works on the
plasticity of expression to produce different phenotypes from similar
genotypes. This is evident even in identical twins.
Norm of Reaction: The degree to which phenotype varies with environmental
We will return to this in more detail, in the Quantitative Genetics portion of the course.
There's more to maternal inheritance than mitochondria and chloroplasts.
Direction of Shell Coiling in Lymnaea, a
The type of inheritance we're about to cover is known as maternal effect--not maternal
In these snails, there are two directions the shell can coil (when you
look at it with the opening facing you:
- dextral (right-handed) is the more common coiling direction
- sinistral (left-handed) is the rarer direction
(Side note: These snails are hermaphroditic, each having both male and female sex organs. So any given snail can play the part of male or female and donate either eggs or sperm to the next generation. The scientist can thus decide which snails to allow to be the mother or the father. We also have the luxury of allowing them to self-fertilize.)
If you cross...
- female dex x male sin the F1 will be 100% dextral
- If you allow the F1 to self-fertilize, the F2 is 100% dextral.
- What you'd expect, though, if this were a normal, Mendelian trait, is
a 3:1 ratio of dex: sin.
If you cross...
- male dex x female sin the F1 will be 100% sinistral
- If you allow these to self-fertilize, the F2 will be 100% dextral!
Turns out that the phenotype of the offspring depends on the genotype of
the mother snail. This is known as maternal effect.
The coiling direction of a particular individual's shell is governed by its
Why does this happen?
spiral cleavage direction is due to the tilt of the mitotic spindle
left) with respect to the direction of the animal/vegetal axis.
the tilt direction is governed by the mother's cytoplasm, which is, in
turn, controlled by her nuclear DNA.
the ovum contains maternal cytoplasm. Hence, the direction of the baby snail's shell coiling is determined, not by its own genes, but by the mitotic spindle of it's mother's cytoplasmic legacy.
Here are all the possibilities:
No matter which direction her own shell coils, a DD or Dd mother snail will always produce right-tilting ova. All her babies will be dextral.
No matter which direction her own shell coils, a dd mother snail will always produce left-tilting ova. All her babies will be sinistral.
Maternal effect is also seen in larval development of Ephestia kuehniella,
the Flour Moth:
kynurenin is a precursor to a particular type of
dominant allele (a+) codes for pigment;
recessive allele (a) codes for no pigment. (Mutant individuals
cannot produce kynurenin, but if they are provided with it, they
can convert it into melanin.)
if you cross:
- pigmented male x nonpigmented female, offspring exhibit
typical Mendelian ratios (depending on the genotype of the male)
if you cross:
- pigmented female x nonpigmented male, offspring are
A pigmented mom (even if she's heterozygous) will
deposit a limited amount of kynurenin in the cytoplasm in the
Even a larva with aa genotype can convert this kynurenin to melanin.
As the larva develops, each instar produces less
melanin, and by the time it's an adult, it has run out of kynurenin.
At this point, it becomes unpigmented.