Genetics 101 (Unit 3 Freshman pre AP Bio) Nedwidek Moore adapted from AP Bio for Frosh Bio Starting March 3 2026 ending 3 26 26

Genetics 101
(Unit 3 Freshman pre AP Bio)
Nedwidek Moore adapted from AP Bio for Frosh Bio
Starting March 3 2026 ending 3 26 26

Ned’s Laws Annotate this and explain steps 6,7,8 below. MEMORIZE THIS PAGE AND THE LEXICON ASAP!

Ned’s Laws
Annotate this and explain steps 6,7,8 below.
MEMORIZE THIS PAGE AND THE LEXICON
ASAP!

Monohybrid: circle F2 outcomes: circle G,P on back of your worksheet: percents or a ratio are OK. T=tall t=short TT x tt (T) (t) F1: Genotype 1Tt or 100 Tt Phenotype 1 Tall or 100 Tall Self F1: Tt x Tt (T, t) (T, t)

Monohybrid: circle F2 outcomes: circle G,P on back
of your worksheet: percents or a ratio are OK.
T=tall t=short
TT x tt
(T) (t)
F1: Genotype 1Tt or 100 Tt Phenotype 1 Tall or 100 Tall
Self F1: Tt x Tt
(T, t) (T, t)

Continued Self F1: Tt x Tt (T, t) (T, t) T t T TT Tt t Tt tt G: 1TT 2Tt 1tt or 25 TT 50 Tt 25 tt P: 3 Tall 1 short or 75 Tall 25 short

Continued
Self F1: Tt x Tt
(T, t) (T, t)
T t
T TT Tt
t Tt tt
G: 1TT 2Tt 1tt or 25 TT 50 Tt 25 tt
P: 3 Tall 1 short or 75 Tall 25 short

Monohybrid period 4 last year: circle F2 outcomes: circle G,P on back of lexicon: percents or a ratio are Ok; you do this on the back of your worksheet. 2 pure parents: T=tall; t=short TT x tt (T) (t) F1: 1Tt or 100% Tt (Genotypes) 1 Tall or 100% Tall Self F1: Tt x Tt (T, t) (T, t)

Monohybrid period 4 last year: circle F2 outcomes:
circle G,P on back of lexicon: percents or a ratio are
Ok; you do this on the back of your worksheet.
2 pure parents: T=tall; t=short
TT x tt
(T) (t)
F1: 1Tt or 100% Tt (Genotypes) 1 Tall or 100% Tall
Self F1: Tt x Tt
(T, t) (T, t)

Continued Self F1: Tt x Tt (T, t) (T, t) T t T TT Tt t Tt tt G: 1TT: 2Tt: 1tt or 25 TT: 50 Tt: 25 tt P: 3 Tall : 1 short or 75 Tall: 25 short

Continued
Self F1: Tt x Tt
(T, t) (T, t)
T t
T TT Tt
t Tt tt
G: 1TT: 2Tt: 1tt or 25 TT: 50 Tt: 25 tt
P: 3 Tall : 1 short or 75 Tall: 25 short

Why is hybrid vigor so important? Dogs and cats Pure breeding: Why do it? Why not do it? Agriculture. Pure strains are inbred to be maintained. Unite to form hybrids bc you can’t keep a hybrid line. Monoculture is a problem, but so can hybrids be. We are hybrid for most traits. “Bad” traits from one parent are covered or patched by good from another. Most traits are not strictly dominant or recessive. Complementary genomes. Genomes must complement each other in hybrid form to protect species survival.

Why is hybrid vigor so important?
Dogs and cats
Pure breeding: Why do it? Why not do it?
Agriculture. Pure strains are inbred to be maintained. Unite to form hybrids bc you
can’t keep a hybrid line.
Monoculture is a problem, but so can hybrids be.
We are hybrid for most traits. “Bad” traits from one parent are covered or patched
by good from another.
Most traits are not strictly dominant or recessive. Complementary genomes.
Genomes must complement each other in hybrid form to protect species survival.

Monohybrid, test cross, dihybrid: what are these? Monohybrid: Aa x Aa: 1AA 2Aa 1aa genos and 3 dominant 1 recessive phenos Test cross 1: AA x aa Vs Test cross 2: Aa x aa distinguishes heterozygosity Test cross 3: AaBb x aabb distinguishes maternal or paternal trait origin. Dihybrid, IA acting: AaBb x AaBb: 1 AABB; 2 AABb; 1AAbb; 2 AaBB; 4 AaBb; 2 Aabb; 2 aaBb; 1 aabb; 1 aaBB (Genos) 9 dominant at A & at B: 3 dom at A rec at b: 3 rec at a dom at B: 1 rec at a & at b (Phenos)

Monohybrid, test cross, dihybrid: what are these?
Monohybrid: Aa x Aa: 1AA 2Aa 1aa genos and 3 dominant 1 recessive phenos
Test cross 1: AA x aa
Vs Test cross 2: Aa x aa distinguishes heterozygosity
Test cross 3: AaBb x aabb distinguishes maternal or paternal trait origin.
Dihybrid, IA acting:
AaBb x AaBb: 1 AABB; 2 AABb; 1AAbb; 2 AaBB; 4 AaBb; 2 Aabb; 2 aaBb; 1 aabb; 1 aaBB (Genos)
9 dominant at A & at B: 3 dom at A rec at b: 3 rec at a dom at B: 1 rec at a & at b (Phenos)

Mendelian Genetics Which of these is a test cross and which a monohybrid and Why? What might a test cross be for?

Mendelian
Genetics
Which of these
is a test cross
and which a
monohybrid and
Why? What might
a test cross be
for?

Mendel’s Laws I : Dominance and Segregation Variation is accidental. The following crosses set up two of mendel’s laws. Expand each with genotypic and phenotypic ratios, and explain which best illustrates dominance and which best illustrates segregation. Use Ned’s Laws. AA x aa and Aa x Aa All dominant pheno about 25% recessive pheno emerges See next page. If the recessive trait is bad this is the prototypical carrier transmission profile for a recessively inherited genetic illness.

Mendel’s Laws I : Dominance and Segregation
Variation is accidental. The following crosses set up two of mendel’s laws.
Expand each with genotypic and phenotypic ratios, and explain which best
illustrates dominance and which best illustrates segregation. Use Ned’s Laws.
AA x aa and Aa x Aa
All dominant pheno about 25% recessive pheno emerges
See next page. If the recessive trait is
bad this is the prototypical carrier
transmission profile for a recessively
inherited genetic illness.

Monohybrid Cross: 2 different traits are allelic

Monohybrid
Cross:
2 different
traits are
allelic

Dihybrid Cross Explain why each trait type needs representation in this cross. What phenomenon do you know of that makes traits assort dependently? Right-most only applies if IA working.

Dihybrid
Cross
Explain why each
trait type needs
representation
in this cross. What
phenomenon do
you know of that
makes traits assort
dependently?
Right-most only
applies if IA working.

Mendel’s Laws 2: Independent Assortment Meiosis shuffles chromosomes through 2 rounds of PMAT. Consider every genetic entity for gamete formation for the following cross. Set it up and carry it through using Ned’s Laws. T is tall t is short height Y is yellow y is green seed. Pd 10 TtYy x TtYy:

Mendel’s Laws 2: Independent Assortment
Meiosis shuffles chromosomes through 2 rounds of PMAT. Consider every genetic entity
for gamete formation for the following cross. Set it up and carry it through using Ned’s
Laws. T is tall t is short height Y is yellow y is green seed. Pd 10
TtYy x TtYy:

Linkage and essential traits All gametes must have all essential traits represented as you need one distinct copy from each parent. Genomes are large. No one trait can live on strictly its own chromosome. Humans have 46 chromosomes and 30,000 genes about, this means each chromosome holds several hundred genes. It also means truly independent assortment of most traits is impossible.

Linkage and essential traits
All gametes must have all essential traits represented as you need one distinct
copy from each parent.
Genomes are large. No one trait can live on strictly its own chromosome.
Humans have 46 chromosomes and 30,000 genes about, this means each
chromosome holds several hundred genes. It also means truly independent
assortment of most traits is impossible.

Dihybrid template: fill in TtYy x TtYy: TY Ty tY ty TY Ty tY ty

Dihybrid template: fill in
TtYy x TtYy:
TY Ty tY ty
TY
Ty
tY
ty

Example 1 TtYy x TtYy: TY Ty tY ty TY TTYY TTYy TtYY TtYy Ty TTYy TTyy TtYy Ttyy tY TtYY TtYy ttYY ttYy ty TtYy Ttyy ttYy ttyy G: 1TTYY: 2TTYy: 2TtYY: 1TTyy: 4TtYy: 2Ttyy: 1ttYY: 2ttYy: 1ttyy P: 9 Tall Yellow: 3 Tall green: 3 short yellow: 1 short green

Example 1
TtYy x TtYy:
TY Ty tY ty
TY TTYY TTYy TtYY TtYy
Ty TTYy TTyy TtYy Ttyy
tY TtYY TtYy ttYY ttYy
ty TtYy Ttyy ttYy ttyy
G: 1TTYY: 2TTYy: 2TtYY: 1TTyy: 4TtYy: 2Ttyy: 1ttYY: 2ttYy: 1ttyy
P: 9 Tall Yellow: 3 Tall green: 3 short yellow: 1 short green

Example 2 TtYy x TtYy: TY Ty tY ty TY TTYY TTYy TtYY TtYy Ty TTYy TTyy TtYy Ttyy tY TtYY TtYy ttYY ttYy ty TtYy Ttyy ttYy ttyy G: 1TTYY: 2TTYy: 2TtYY: 1TTyy: 4TtYy: 2Ttyy: 1ttyy: 2ttYy: 1ttYY P: 9 tall yellow: 3 tall green: 3 short yellow: 1 short green

Example 2
TtYy x TtYy:
TY Ty tY ty
TY TTYY TTYy TtYY TtYy
Ty TTYy TTyy TtYy Ttyy
tY TtYY TtYy ttYY ttYy
ty TtYy Ttyy ttYy ttyy
G: 1TTYY: 2TTYy: 2TtYY: 1TTyy: 4TtYy: 2Ttyy: 1ttyy: 2ttYy: 1ttYY
P: 9 tall yellow: 3 tall green: 3 short yellow: 1 short green

Example 3 TtYy x TtYy: TY Ty tY ty TY TTYY TTYy TtYY TtYy Ty TTYy TTyy TtYy Ttyy tY TtYY TtYy ttYY ttYy ty TtYy Ttyy ttYy ttyy G: 1TTYY: 2TTYy: 1TTyy: 2TtYY: 4TtYy: 2Ttyy: 1ttYY: 2ttYy: 1ttyy P: 9 Tall yellow: 3 Tall green: 3 short yellow: 1 short green

Example 3
TtYy x TtYy:
TY Ty tY ty
TY TTYY TTYy TtYY TtYy
Ty TTYy TTyy TtYy Ttyy
tY TtYY TtYy ttYY ttYy
ty TtYy Ttyy ttYy ttyy
G: 1TTYY: 2TTYy: 1TTyy: 2TtYY: 4TtYy: 2Ttyy: 1ttYY: 2ttYy: 1ttyy
P: 9 Tall yellow: 3 Tall green: 3 short yellow: 1 short green

Example 4 TtYy x TtYy: TY Ty tY ty TY TTYY TTYy TtYY TtYy Ty TTYy TTyy TtYy Ttyy tY TtYY TtYy ttYY ttYy ty TtYy Ttyy ttYy ttyy G: 1TTYY: 2TTYy: 1TTyy: 2TtYY: 4TtYy: 2Ttyy: 1ttYY: 2ttYy:1ttyy P: 9 Tall Yellow: 3 tall green: 3 short yellow: 1 short green

Example 4
TtYy x TtYy:
TY Ty tY ty
TY TTYY TTYy TtYY TtYy
Ty TTYy TTyy TtYy Ttyy
tY TtYY TtYy ttYY ttYy
ty TtYy Ttyy ttYy ttyy
G: 1TTYY: 2TTYy: 1TTyy: 2TtYY: 4TtYy: 2Ttyy: 1ttYY: 2ttYy:1ttyy
P: 9 Tall Yellow: 3 tall green: 3 short yellow: 1 short green

Example 5 TtYy x TtYy: (TY, Ty, tY, ty) (TY, Ty, tY, ty) TY Ty tY ty TY TTYY TTYy TtYY TtYy P: 9 TALYEL 3 TALgrn 3 shYEL 1shgrn Talyel talyel talyel talyel Ty TTYy TTyy TtYy Ttyy Talyel talgrn talyel talgrn tY TtYY TtYy ttYY ttYy Talyel talyel shyel shyel ty TtYy Ttyy ttYy ttyy Talyel talgrn shyel shgrn

Example 5
TtYy x TtYy:
(TY, Ty, tY, ty) (TY, Ty, tY, ty)
TY Ty tY ty
TY TTYY TTYy TtYY TtYy P: 9 TALYEL 3 TALgrn 3 shYEL 1shgrn
Talyel talyel talyel talyel
Ty TTYy TTyy TtYy Ttyy
Talyel talgrn talyel talgrn
tY TtYY TtYy ttYY ttYy
Talyel talyel shyel shyel
ty TtYy Ttyy ttYy ttyy
Talyel talgrn shyel shgrn

Example 5 TtYy x TtYy: (TY, Ty, tY, ty) (TY, Ty, tY, ty) TY Ty tY ty TY TTYY TTYy TtYY TtYy p: 9 TALYEL 3 TALgrn 3 shYEL 1shgrn Talyel talyel talyel talyel Ty TTYy TTyy TtYy Ttyy Talyel talgrn talyel talgrn tY TtYY TtYy ttYY ttYy Talyel talyel shyel shyel ty TtYy Ttyy ttYy ttyy Talyel talgrn shyel shgrn

Example 5
TtYy x TtYy:
(TY, Ty, tY, ty) (TY, Ty, tY, ty)
TY Ty tY ty
TY TTYY TTYy TtYY TtYy p: 9 TALYEL 3 TALgrn 3 shYEL 1shgrn
Talyel talyel talyel talyel
Ty TTYy TTyy TtYy Ttyy
Talyel talgrn talyel talgrn
tY TtYY TtYy ttYY ttYy
Talyel talyel shyel shyel
ty TtYy Ttyy ttYy ttyy
Talyel talgrn shyel shgrn

What ratio patterns do you see in the 9:3:3:1? AaBb (male parent) x AaBb (female parent) (cross) (AB, Ab, aB, ab) (AB, Ab, aB, ab) AB Ab aB ab AB AABB AABb AaBB AaBb Ab AABb AAbb AaBb Aabb aB AaBB AaBb aaBB aaBb ab AaBb Aabb aaBb aabb State the phenotypic ratio for this (general). State any patterns you see for the A trait versus the B trait as they group together in forming the phenotypic ratios that would be borne out by this cross.

What ratio patterns do you see in the 9:3:3:1?
AaBb (male parent) x AaBb (female parent) (cross)
(AB, Ab, aB, ab) (AB, Ab, aB, ab)
AB Ab aB ab
AB AABB AABb AaBB AaBb
Ab AABb AAbb AaBb Aabb
aB AaBB AaBb aaBB aaBb
ab AaBb Aabb aaBb aabb
State the phenotypic ratio for this (general). State any patterns you see for the A
trait versus the B trait as they group together in forming the phenotypic ratios that
would be borne out by this cross.

Offspring Patterns continued For a given dihybrid cross of the form AaBb x AaBb, expect the following phenotypes 9 dominant expression at locus 1 dominant expression at locus 2 3 dominant expression at locus 1 recessive expression at locus 2 3 recessive expression at locus 1 dominant expression at locus 2 1 recessive expression at locus 1 recessive expression at locus 2

Offspring Patterns continued
For a given dihybrid cross of the form AaBb x AaBb, expect the following
phenotypes
9 dominant expression at locus 1 dominant expression at locus 2
3 dominant expression at locus 1 recessive expression at locus 2
3 recessive expression at locus 1 dominant expression at locus 2
1 recessive expression at locus 1 recessive expression at locus 2

Meiosis and Variation (revisit again w/ Evolution) Sexual Reproduction imparts variation by three key mechanisms: Crossovers at early prophase. Shuffling by Independent Assortment of genetic material at gametogenesis. Random aspects of what maternal gamete fertilizes what paternal gamete. These events are complicated and costly to do, so why are these three elements so important that they are retained? Because they allow genomes to diversify enough to survive environmental strain. Hybrid vigor is a goal . Heterozygote advantage is related to this. Wild type alleles are the most common or prevalent natural forms of an allele in a population.

Meiosis and Variation (revisit again w/ Evolution)
Sexual Reproduction imparts variation by three key mechanisms:
Crossovers at early prophase.
Shuffling by Independent Assortment of genetic material at gametogenesis.
Random aspects of what maternal gamete fertilizes what paternal gamete.
These events are complicated and costly to do, so why are these three elements
so important that they are retained? Because they allow genomes to
diversify enough to survive environmental strain.
Hybrid vigor is a goal . Heterozygote advantage is related to this.
Wild type alleles are the most common or prevalent natural forms of an allele
in a population.

Atypical Mendelian: Which is Incomplete and which Codominance?

Atypical Mendelian:
Which is Incomplete and which Codominance?

Simple Atypical inheritance: Please use Ned’s Laws: Allelic Gene Interactions Blood types: AO x BO Yields: Four O’clocks: RR (red) X WW (white) Yields: RW (pink) Self F1 then express the final g and p ratios for F2 only: AB AO BO OO G F1: RW RW x RW AB A B O p F2 G: 1RR 2RW 1WW Set up and memorize F2 P: 1 RED 2 PINK 1 WHITE AO x BO g,p RW x RW g,p Andalusian Fowl Follow the same patterns with BW x BW g, p the pure birds being black (BB) and white (WW) and the intermediate being speckled blue (BW).

Simple Atypical inheritance: Please use Ned’s
Laws: Allelic Gene Interactions
Blood types: AO x BO Yields: Four O’clocks: RR (red) X WW (white) Yields: RW (pink)
Self F1 then express the final g and p ratios for F2 only:
AB AO BO OO G F1: RW RW x RW
AB A B O p F2 G: 1RR 2RW 1WW
Set up and memorize F2 P: 1 RED 2 PINK 1 WHITE
AO x BO g,p RW x RW g,p Andalusian Fowl Follow the same patterns with
BW x BW g, p the pure birds being black (BB) and white (WW)
and the intermediate being speckled blue (BW).

Simple Atypicals: Please use Ned’s Laws. Blood types: AO x BO Yields: Four O clocks: RR (red) X WW (white) Yields: RW (pink) Self F1 then express the final g and p ratios for F2 only: AB AO BO OO g F1: RW: cross two siblings: RW x RW AB A B O p F2: 1RR 2RW 1WW g Background 1 red 2 pink 1 white p Phenotypes Andalusian Fowl Follow the same patterns with Discuss the pure birds being black (BB) and white (WW) and the intermediate being speckled blue (BW).

Simple Atypicals: Please use Ned’s Laws.
Blood types: AO x BO Yields: Four O clocks: RR (red) X WW (white) Yields: RW (pink)
Self F1 then express the final g and p ratios for F2 only:
AB AO BO OO g F1: RW: cross two siblings: RW x RW
AB A B O p F2: 1RR 2RW 1WW g
Background 1 red 2 pink 1 white p
Phenotypes Andalusian Fowl Follow the same patterns with
Discuss the pure birds being black (BB) and white (WW)
and the intermediate being speckled blue (BW).

Human Characteristics Genetically Normal humans have 44 autosomes + XX (female) (repeated again later) 44 autosomes +XY (male) Females knock out 1 X for balance in a phenomenon called dosage compensation. The knockout chromosome is heterochromatin. Accessible genes are euchromatin, or true chromatin. A genetic disease is when every single cell has a mistake in its code that causes those cells to malfunction. Typically, it is one gene or a group of genes. Some of these diseases inherit in a Mendelian way (4 major inheritance patterns) and some not (chromosome abnormalities, multigenic disorders (multiple genes create a particular outcome), pleiotropy (one gene two effects)).

Human Characteristics Genetically
Normal humans have 44 autosomes + XX (female) (repeated again later)
44 autosomes +XY (male)
Females knock out 1 X for balance in a phenomenon called dosage compensation.
The knockout chromosome is heterochromatin. Accessible genes are euchromatin,
or true chromatin.
A genetic disease is when every single cell has a mistake in its code that causes
those cells to malfunction. Typically, it is one gene or a group of genes. Some of
these diseases inherit in a Mendelian way (4 major inheritance patterns) and some
not (chromosome abnormalities, multigenic disorders (multiple genes create a
particular outcome), pleiotropy (one gene two effects)).

4 major Mendelian inheritance patterns AD AUTOSOMAL DOMINANT AR AUTOSOMAL RECESSIVE XD X LINKED DOMINANT XR X LINKED RECESSIVE How many alleles are possible at a given locus for a given trait? (2 or more) What does allelic mean? (same spot on each of two homologous chromosomes). https://pmc.ncbi.nlm.nih.gov/articles/PMC4029837/ See top of paragraph 4 regarding allelic heterogeneity in CFTR mutations (2000+).

4 major Mendelian inheritance patterns
AD AUTOSOMAL DOMINANT
AR AUTOSOMAL RECESSIVE
XD X LINKED DOMINANT
XR X LINKED RECESSIVE
How many alleles are possible at a given locus for a given trait? (2 or more) What
does allelic mean? (same spot on each of two homologous chromosomes).
https://pmc.ncbi.nlm.nih.gov/articles/PMC4029837/
See top of paragraph 4 regarding allelic heterogeneity in CFTR mutations (2000+).

Sex Linkage prompt Notation for sex-linked recessive disease in humans: Hemophilia is X-linked recessive: use superscript notation as previously discussed. Conventional Key, X-linked recessive: X A = normal, X a = affected, Y = Y

Sex Linkage prompt
Notation for sex-linked recessive disease in humans:
Hemophilia is X-linked recessive: use superscript notation as previously discussed.
Conventional Key, X-linked recessive:
X A = normal, X a = affected, Y = Y

V 1 X A X a x X A Y X A X a X A X A X A X A X a Y X A Y X a Y X A X a x X a Y X A X a X a X A X a X a X a Y X A Y X a Y

V 1
X A X a x X A Y
X A X a
X A X A X A X A X a
Y X A Y X a Y
X A X a x X a Y
X A X a
X a X A X a X a X a
Y X A Y X a Y

V 2 X A X a x X A Y X A X a X A X A X A X A X a Y X A Y X a Y X A X a x X a Y X A X a X a X A X a X a X a Y X A Y X a Y

V 2
X A X a x X A Y
X A X a
X A X A X A X A X a
Y X A Y X a Y
X A X a x X a Y
X A X a
X a X A X a X a X a
Y X A Y X a Y

Outcomes: Genotypes Carrier x normal male: G: X A X A X A X a X A Y X a Y Carrier x sick male: G: X A X a X a X a X A Y X a Y

Outcomes: Genotypes
Carrier x normal male:
G: X A X A X A X a X A Y X a Y
Carrier x sick male:
G: X A X a X a X a X A Y X a Y

Phenotypes Carrier x normal male P: 1 normal female: 1 carrier female: 1 normal male: 1 affected male Carrier x affected male P: 1 carrier female: 1 affected female: 1 normal male: 1 affected male Males are more likely to show X rec diseases bc there is no homolog to cover up such alleles

Phenotypes
Carrier x normal male
P: 1 normal female: 1 carrier female: 1 normal male: 1 affected male
Carrier x affected male
P: 1 carrier female: 1 affected female: 1 normal male: 1 affected male
Males are more likely to show X rec diseases bc there is no homolog to cover up
such alleles

Phenotypes again, with context Carrier x normal male phenotypes 1 normal female: 1 carrier female: 1 normal male: 1 affected male Carrier x affected male phenotypes 1 carrier female: 1 affected female: 1 normal male: 1affected male For sex linked recessive traits, risk is higher for male inheritance. Why? Because male only gets one X (no hybrid vigor). For instance if mom carries a defective X, she has a 50 percent chance of having a sick son. If Y linked, only males can get sick.

Phenotypes again, with context
Carrier x normal male phenotypes
1 normal female: 1 carrier female: 1 normal male: 1 affected male
Carrier x affected male phenotypes
1 carrier female: 1 affected female: 1 normal male: 1affected male
For sex linked recessive traits, risk is higher for male inheritance. Why? Because
male only gets one X (no hybrid vigor). For instance if mom carries a defective X,
she has a 50 percent chance of having a sick son. If Y linked, only males can get
sick.

From sex linkage to all linkage: Summary of Ideas Sex linked genes localize to the X chromosome. Two or more traits can be linked to each other on any chromosome. If that is the case, we should be able to map their position and distance relative to one another, to the telomeres and to the centromere. Human chromosomes have two “arms”, p and q. When chromosomes are distributed to 2 new cells after replication and division, they decondense a little and are considered ready to be accessed. We visualize chromosome content with either linear (animal and plant) or circular (bacteria and organellar) maps of the gene locations..

From sex linkage to all linkage: Summary of Ideas
Sex linked genes localize to the X chromosome.
Two or more traits can be linked to each other on any chromosome.
If that is the case, we should be able to map their position and distance relative to
one another, to the telomeres and to the centromere. Human chromosomes have
two “arms”, p and q.
When chromosomes are distributed to 2 new cells after replication and division,
they decondense a little and are considered ready to be accessed. We visualize
chromosome content with either linear (animal and plant) or circular (bacteria and
organellar) maps of the gene locations..

Lab schedule etc next few weeks Hold on to relationships and biodiversity for week we return. Running 4 13->4 16 Test is monday march 30 2026 all mendelian March 30 2026 is also an A pushin day in room 717. Period 5 will stay thru 6th after their exam (ex time students will return from holding area) and period 9 will arrive early to 717 at the start of period 8 (ex time students will leave for the holding room beginning period 9)

Lab schedule etc next few weeks
Hold on to relationships and biodiversity for week we return. Running 4 13->4 16
Test is monday march 30 2026 all mendelian
March 30 2026 is also an A pushin day in room 717. Period 5 will stay thru 6th
after their exam (ex time students will return from holding area) and period 9 will
arrive early to 717 at the start of period 8 (ex time students will leave for the
holding room beginning period 9)

Intro to mapping (this is not in shared handouts) How do we know genes are linked? Initially we do not. We assume independent assortment of the two traits initially … WHY????? AaBb x aabb test cross between brown curly and white straight (AB, Ab, aB, ab) (ab) haploid gametes If the a trait is not linked to the b trait, in other words these traits assort independently, what do we predict?? Offspring genotypes: 1AaBb, 1Aabb, 1aaBb, 1aabb A encodes brown, a encodes white, B encodes curly, b encodes straight Offspring phenotypes: 1 brown curly, 1 brown straight, 1 white curly, 1 white straight WHAT ARE THE TWO TRAITS? If the a trait is linked to the b trait, what do we predict (one possibility): Parent 1 (het) is A B a b This is a cis (same strand) arrangement of wild type alleles; the big alleles are tethered and assume they are wild type. Parent 2 is a b a b first we establish that the genes are tethered then we go in and figure out how far they are from one another. What is the majority offspring phenotype here? what are the minor phenotypes, and why?

Intro to mapping (this is not in shared handouts)
How do we know genes are linked? Initially we do not. We assume independent assortment of the two traits initially … WHY?????
AaBb x aabb test cross between brown curly and white straight
(AB, Ab, aB, ab) (ab) haploid gametes
If the a trait is not linked to the b trait, in other words these traits assort independently, what do we predict??
Offspring genotypes: 1AaBb, 1Aabb, 1aaBb, 1aabb
A encodes brown, a encodes white, B encodes curly, b encodes straight
Offspring phenotypes: 1 brown curly, 1 brown straight, 1 white curly, 1 white straight WHAT ARE THE TWO TRAITS?
If the a trait is linked to the b trait, what do we predict (one possibility):
Parent 1 (het) is
A B
a b This is a cis (same strand) arrangement of wild type alleles; the big alleles are tethered and assume they are wild type.
Parent 2 is
a b
a b
first we establish that the genes are tethered then we go in and figure out how far they are from one another. What is the majority
offspring phenotype here? what are the minor phenotypes, and why?

Linkage Testcross: two traits

Linkage
Testcross:
two traits

Cis and Trans orientation

Cis and Trans orientation

A mapping problem I crossed a brown curly parent with a white straight parent. I got these offspring outcomes which are not what I predicted based on linkage. Parental ditypes are the big numbers. Nonparental ditypes or recombinants are the small numbers. Linked genes by definition are physically tethered on the same chromosome. Map units apart are a function of the percentage of recombinants within a large offspring population such as below. Genes move together more often the closer they are to each other. Genes on opposite sides of the centromere (p or q arm) almost act like they are on different chromosomes. AaBb: 749: brown curly aabb: 751: white straight Aabb: 251: brown straight aaBb: 249: white curly How far are color and kink apart and what is the arrangement of alleles in the original parent? Show work.

A mapping problem
I crossed a brown curly parent with a white straight parent. I got these offspring outcomes which are not
what I predicted based on linkage.
Parental ditypes are the big numbers. Nonparental ditypes or recombinants are the small numbers.
Linked genes by definition are physically tethered on the same chromosome. Map units apart are a
function of the percentage of recombinants within a large offspring population such as below. Genes
move together more often the closer they are to each other. Genes on opposite sides of the centromere
(p or q arm) almost act like they are on different chromosomes.
AaBb: 749: brown curly
aabb: 751: white straight
Aabb: 251: brown straight
aaBb: 249: white curly
How far are color and kink apart and what is the arrangement of alleles in
the original parent? Show work.

Math Calculating the Recombination Frequency (RF) (251+249)/2000= 0.25. This is 25%, 25 map units (MU), so kink and color are that far apart. How do we establish the parental or original arrangement of alleles? Look at the largest population: parental ditypes are brown curly, so A and B were on the same strand in the original parent as were a and b.

Math
Calculating the Recombination Frequency (RF)
(251+249)/2000= 0.25. This is 25%, 25 map units (MU), so kink and color are that
far apart.
How do we establish the parental or original arrangement of alleles?
Look at the largest population: parental ditypes are brown curly, so A and B were
on the same strand in the original parent as were a and b.

Linkage at a Glance: Two traits only

Linkage at a Glance:
Two traits only

Linkage of multiple traits on any chromosome Mapping problem page 1 p/u period 1 (in h/o) Purple eye and vestigial wing are linked in fruit flies. If I cross a double heterozygote for purple and vestigial (wild type heterozygous female) with a purple vestigial fly (tester male), I get the following offspring: Nonparental ditypes 157 normal (wild type, both dominant) 146 vestigial purple (recessive, both) parental ditypes: I know these are parental bc of one key bit of information: they are big numbers relative to the total. 965 vestigial normal eye 1067 purple normal wing How far apart are the purple and vestigial mutations, and what arrangement do they assume on the diploid heterozygous mother?

Linkage of multiple traits on any chromosome
Mapping problem page 1 p/u period 1 (in h/o)
Purple eye and vestigial wing are linked in fruit flies. If I cross a double heterozygote for purple and vestigial (wild type
heterozygous female) with a purple vestigial fly (tester male), I get the following offspring:
Nonparental ditypes
157 normal (wild type, both dominant)
146 vestigial purple (recessive, both)
parental ditypes: I know these are parental bc of one key bit of information: they are big numbers relative to the total.
965 vestigial normal eye
1067 purple normal wing
How far apart are the purple and vestigial mutations, and what arrangement do they assume on the diploid heterozygous mother?

Linkage of multiple traits on any chromosome mapping problem page 2 (answer) (in h/o) Purple eye and vestigial wing are linked in fruit flies. If I cross a double heterozygote for purple eye and vestigial wing (wild type heterozygous female) with a purple vestigial fly (tester male), I get the following 2335 offspring: Nonparental ditypes 157 normal (wild type, both dom) 146 vestigial purple (recessive, both) parental ditypes: I know these are parental bc of one key bit of information: Parental ditypes refer to the classes of offspring from a testcross that most resemble the parents at the two loci (or more) being characterized: 965 vestigial normal is assumed for eye 1067 purple normal is assumed for wing (157+146)/2335: 13% RF which translates to 13 MU Trans . What would I need to determine which gene comes “first” in a map?

Linkage of multiple traits on any chromosome
mapping problem page 2 (answer) (in h/o)
Purple eye and vestigial wing are linked in fruit flies.
If I cross a double heterozygote for purple eye and vestigial wing (wild type heterozygous female) with a purple vestigial fly (tester
male), I get the following 2335 offspring:
Nonparental ditypes
157 normal (wild type, both dom)
146 vestigial purple (recessive, both)
parental ditypes: I know these are parental bc of one key bit of information: Parental ditypes refer to the classes of offspring from a
testcross that most resemble the parents at the two loci (or more) being characterized:
965 vestigial normal is assumed for eye
1067 purple normal is assumed for wing
(157+146)/2335: 13% RF which translates to 13 MU Trans . What would I need to determine which gene comes “first” in a map?

Mapping ideas: expect to finish by 3/25 (in h/o) RF for a heterozygous mating with a fully recessive individual is the NPD over the total offspring for a given mating. A proper map needs a third trait for reference. The farther two genes are apart, the higher the RF. The closer two genes are together, the lower the RF. recombination frequency. Genes at distal ends of chromosomes behave almost as though they are assorting independently bc they can go either way. A given map distance breaks down into two even recombination frequencies, the sum of which represent the crossovers between two genes. So if you are given a distance of 10 map units between two genes, this breaks down into two recombinant frequency classes of 5% each. This is because there are two strands segregating. Dominant genes can link on same (cis) or opposite (trans) strands of genome.

Mapping ideas: expect to finish by 3/25 (in h/o)
RF for a heterozygous mating with a fully recessive individual is the NPD over the
total offspring for a given mating. A proper map needs a third trait for reference.
The farther two genes are apart, the higher the RF.
The closer two genes are together, the lower the RF. recombination frequency.
Genes at distal ends of chromosomes behave almost as though they are assorting
independently bc they can go either way.
A given map distance breaks down into two even recombination frequencies, the sum
of which represent the crossovers between two genes. So if you are given a distance
of 10 map units between two genes, this breaks down into two recombinant
frequency classes of 5% each. This is because there are two strands segregating.
Dominant genes can link on same (cis) or opposite (trans) strands of genome.

Pedigrees: Notation: Multiple pedigree handouts Open circle = female unaff Open square = male unaff Shaded circle = female aff Shaded square = male aff Horizontal connections between two shapes are matings. Vertical connections suspended off of a horizontal connection are offspring. There are more symbols in the pedigrees pdf posted. Consanguinity sometimes a double line; look for circuit closure. What does a pedigree represent?

Pedigrees: Notation: Multiple pedigree handouts
Open circle = female unaff
Open square = male unaff
Shaded circle = female aff
Shaded square = male aff
Horizontal connections between two shapes are matings.
Vertical connections suspended off of a horizontal connection are offspring.
There are more symbols in the pedigrees pdf posted. Consanguinity sometimes a
double line; look for circuit closure.
What does a pedigree represent?

Identifying Parts of a Pedigree, Birth Order & Gen’s Put a heart over the gen 1 mating. Purple dot: affected female gen 1. Green flag: affected male gen 2. Blue pin: unaffected male gen 2. Yellow star: unaffected female gen 3. Mate III-2 with III-4. What is that called? Source: https://www.khanacademy.org/science/high-school-biology/hs-classical-genetics/h s-pedigrees/e/hs-pedigrees

Identifying Parts of a Pedigree, Birth Order & Gen’s
Put a heart over the gen 1 mating.
Purple dot: affected female gen 1.
Green flag: affected male gen 2.
Blue pin: unaffected male gen 2.
Yellow star: unaffected female gen 3.
Mate III-2 with III-4. What is that called?
Source:
https://www.khanacademy.org/science/high-school-biology/hs-classical-genetics/h
s-pedigrees/e/hs-pedigrees

Identifying Pedigree, Gen's Birth Parts of Order & a mating. Put heart the a gen 1 over 見 Purple 1 dot: affected 2 female 1. gen 2€ Green flag: affected male gen P 2. pin: Blue unaffected male gen 2. 1 2 3 4 5 Yellow unaffected star: female gen 3. Mate III-2 with III-4. What is that called? 4 Source: 5 6 1 2 3 https://www.khanacademy.org/science/high-school-biology/hs-classical-genetics/h s-pedigrees/e/hs-pedigrees Source: www.khanacademy.or Pear Deck Interactive Slide Students, drag the icons! .. Do not remove this bar

Identifying Pedigree, Birth Gen's
Parts of Order &
a
mating.
Put a heart over the gen 1
見
Purple dot: affected female gen 1. 1 2
2€
Green flag: affected male gen 2. P
pin:
Blue unaffected male gen 2.
1 2 3 4 5
Yellow star: unaffected female gen 3.
Mate III-2 with III-4. What is that called?
Source: 1 2 3 4 5 6
https://www.khanacademy.org/science/high-school-biology/hs-classical-genetics/h
s-pedigrees/e/hs-pedigrees
Source: www.khanacademy.or
Students, drag the icons! Pear Deck Interactive Slide
.. Do not remove this bar

Haploid and Diploid Patterning: Recessive Autosomal recessive Haploids A = normal/ok/unaffected a = not ok/affected Diploids: A/- = normal/unaffected note: carriers don’t usually manifest (demonstrate) aa = affected X-linked recessive Haploids X A = unaffected X a = affected Y = Y Diploids Females X A X A = unaffected female X A X a = unaffected female carrier X a X a = affected female Males X A Y = unaffected male X a Y = affected male From what you know about X inactivation, could a female carrier here manifest a phenotype?

Haploid and Diploid Patterning: Recessive
Autosomal recessive Haploids A = normal/ok/unaffected a = not ok/affected
Diploids: A/- = normal/unaffected note: carriers don’t usually manifest (demonstrate) aa = affected
X-linked recessive Haploids X A = unaffected X a = affected Y = Y
Diploids
Females X A X A = unaffected female
X A X a = unaffected female carrier
X a X a = affected female
Males X A Y = unaffected male
X a Y = affected male
From what you know about X inactivation, could a female carrier here manifest a phenotype?

Haploid and Diploid Patterning: Dominant Autosomal Dominant H: A = affected a = unaffected D: A/- = affected aa = unaffected X-linked Dominant Hap X A = affected X a = unaffected Y = Y Diploid Females X A X A = affected female X A X a = affected female X a X a = unaffected female Diploid Males X A Y = affected male X a Y = unaffected male X linked Dominant diseases are not on the list of ones to memorize. Why are they so rare?

Haploid and Diploid Patterning: Dominant
Autosomal Dominant
H: A = affected a = unaffected
D: A/- = affected aa = unaffected
X-linked Dominant
Hap X A = affected X a = unaffected Y = Y
Diploid Females
X A X A = affected female
X A X a = affected female
X a X a = unaffected female
Diploid Males
X A Y = affected male
X a Y = unaffected male X linked Dominant diseases are not on the list of ones to memorize. Why are they so rare?

Pedigrees: Hallmarks It would be a help if you know 4 major types of Mendelian inheritance pattern pedigree hallmarks. Explain each of these points using the pedigree file you were given. Auto Recessive (AR): Parents of an affected kid are usually carriers (unaffected, not sick). Auto Dominant (AD): Usually shows an affect every generation. X recessive (XR): High incidence of affected males and carrier females. X dominant (XD): affected males with normal mates have no affected sons and no normal daughters.

Pedigrees: Hallmarks
It would be a help if you know 4 major types of Mendelian inheritance pattern pedigree
hallmarks. Explain each of these points using the pedigree file you were given.
Auto Recessive (AR): Parents of an affected kid are usually carriers (unaffected, not sick).
Auto Dominant (AD): Usually shows an affect every generation.
X recessive (XR): High incidence of affected males and carrier females.
X dominant (XD): affected males with normal mates have no affected sons and no normal
daughters.

Pedigrees at a Glance: Companion punnetts For pedigree diagrams And quick reference For normal and affected Outcomes for Mendelian genetic Disease transmission

Pedigrees at a Glance:
Companion punnetts
For pedigree diagrams
And quick reference
For normal and affected
Outcomes for
Mendelian genetic
Disease transmission

AR

AD

XR

XD

Patterns on pdf for pedigrees (only for fun) Pedigrees: Setup cross, assess agreement. AD Huntingtons: note manifestation: lose cognition, motor. Late onset DARK HEART 1: Aa x aa yes meets with pred OPEN HEART 2: Aa x Aa not enough info to assess AR Albinism: note manifestation: no pigment, vulnerable to skin damage DARK HEART 1: AA x aa yes meets with prediction OPEN HEART 2: Aa x Aa no ped does not meet with prediction XD inherited Rickets: note manifestation: soft bones DARK HEART 1: X A Y x X a X a yes ped does agree OPEN HEART 2: yes does agree XR Duchenne's Muscular Dystrophy: note manifestation: muscle weakness, motor degeneration DARK HEART 1: X A Y x X A X a : ped does not precisely agree OPEN HEART 2: X A X A x X a Y: no way to tell agreement Why are pedigree outcomes not necessarily like straight Punnetts?

Patterns on pdf for pedigrees (only for fun)
Pedigrees: Setup cross, assess agreement.
AD Huntingtons: note manifestation: lose cognition, motor. Late onset
DARK HEART 1: Aa x aa yes meets with pred
OPEN HEART 2: Aa x Aa not enough info to assess
AR Albinism: note manifestation: no pigment, vulnerable to skin damage
DARK HEART 1: AA x aa yes meets with prediction
OPEN HEART 2: Aa x Aa no ped does not meet with prediction
XD inherited Rickets: note manifestation: soft bones
DARK HEART 1: X A Y x X a X a yes ped does agree
OPEN HEART 2: yes does agree
XR Duchenne's Muscular Dystrophy: note manifestation: muscle weakness, motor degeneration
DARK HEART 1: X A Y x X A X a : ped does not precisely agree
OPEN HEART 2: X A X A x X a Y: no way to tell agreement
Why are pedigree outcomes not necessarily like straight Punnetts?

Pedigrees and Key Diseases: Review, all classes Some important Diseases: Mendelian: Cystic fibrosis (AR) lung disease targets channels: Cl- ion flow. Lo life expectancy without transplant. Tay-sachs (AR) neuro and lethal by age 5 (worst kind), a few milder kinds. Lysosomal storage fail; excess lipids cause neuro damage Sickle Cell Anemia (AR) : Heterozygote advantage in certain places. Painful attacks if two defective genes. Huntingtons (AD) : neuro, late onset 40s, degenerative, lethal; buildup of defective protein; more repeats earlier onset Achondroplasia (AD) (not required for AP, but Ned put fascinating fact test question): DWARFISM: There is a test question … Double dominants are lethal and two dwarves can have a normal child. Why? Duchennes MD (XR) : neuromuscular, gait and mobility problems. Dystrophin is huge and easy to destroy by mutation; many lesions possible. Short life expectancy. Hemophilia (XR) : clotting disorder. Treatable hemophilia A and B are the 2 major types. From a few slides ago: female carr x norm male: 1X A X A :1X A X a : 1X A Y: 1X a Y Female carrier x affected male: 1X A X a :1X a X a :1X A Y: 1X a Y Question : Why do genetic diseases “skip” generations when they’re recessive? What are these diseases caused by?

Pedigrees and Key Diseases: Review, all classes
Some important Diseases: Mendelian:
Cystic fibrosis (AR) lung disease targets channels: Cl- ion flow. Lo life expectancy without transplant.
Tay-sachs (AR) neuro and lethal by age 5 (worst kind), a few milder kinds. Lysosomal storage fail;
excess lipids cause neuro damage
Sickle Cell Anemia (AR) : Heterozygote advantage in certain places. Painful attacks if two defective
genes.
Huntingtons (AD) : neuro, late onset 40s, degenerative, lethal; buildup of defective protein; more
repeats earlier onset
Achondroplasia (AD) (not required for AP, but Ned put fascinating fact test question): DWARFISM:
There is a test question … Double dominants are lethal and two dwarves can have a normal child.
Why?
Duchennes MD (XR) : neuromuscular, gait and mobility problems. Dystrophin is huge and easy to
destroy by mutation; many lesions possible. Short life expectancy.
Hemophilia (XR) : clotting disorder. Treatable hemophilia A and B are the 2 major types.
From a few slides ago: female carr x norm male: 1X A X A :1X A X a : 1X A Y: 1X a Y
Female carrier x affected male: 1X A X a :1X a X a :1X A Y: 1X a Y
Question : Why do genetic diseases “skip” generations when they’re recessive? What are these diseases caused by?

Pedigrees Key Diseases: Review, and all classes Mendelian: Autosomal Mendelian: Autosomal Mendelian: X-Linked (AR) Dominant (AD) (XR) Recessive Recessive Cystic Fibrosis: lung Huntingtons: Duchennes disease neuro, late MD: targets channels: Cl- flow. ion Lo onset 40s, degenerative, neuromuscular, gait and life expectancy without transplant. buildup lethal; of defective mobility problems. Dystrophin protein; repeats more earlier by is huge and easy to destroy onset. mutation; many lesions Tay-Sachs: lethal by and neuro possible. Short life expectancy. (worst kind), age 5 few milder Achondroplasia: a kinds. Lysosomal storage fail; DWARFISM: There is test a Hemophilia: clotting lipids excess cause question... Double dominants neuro disorder. Treatable hemophilia damage. lethal and are two dwarves can types. A and B are the 2 major have normal child. Why? a Sickle Cell Anemia: Heterozygote advantage in Genotypes (Review): places. certain Painful attacks if female male: 1XAXA:1XAXa: 1XAY: 1X³Y carr x norm two defective genes. Female carrier affected male: 1XAXa:1XaXa:1XAY: 1XaY x by? Question: Why do genetic diseases "skip" generations when they're recessive? What these diseases caused are Pear Deck Interactive Slide Students, anywhere draw this slide! on Do not remove this bar

Pedigrees and Key Diseases: Review, all classes
Mendelian: Autosomal Mendelian: Autosomal Mendelian: X-Linked
Recessive (AR) Dominant (AD) Recessive (XR)
Cystic Fibrosis: lung disease Huntingtons: neuro, late Duchennes MD:
targets channels: Cl- ion flow. Lo onset 40s, degenerative, neuromuscular, gait and
life expectancy without transplant. lethal; buildup of defective mobility problems. Dystrophin
protein; more repeats earlier is huge and easy to destroy by
onset. mutation; many lesions
Tay-Sachs: and lethal by
neuro possible. Short life expectancy.
age 5 (worst kind), a few milder Achondroplasia:
kinds. Lysosomal storage fail; DWARFISM: There is a test
Hemophilia: clotting
lipids
excess cause neuro question... Double dominants disorder. Treatable hemophilia
damage. are lethal and two dwarves can
A and B are the 2 major types.
have normal child. Why?
a
Sickle Cell Anemia:
Heterozygote advantage in
Genotypes (Review):
certain places. Painful attacks if
female carr x norm male: 1XAXA:1XAXa: 1XAY: 1X³Y
two defective genes.
Female carrier affected male: 1XAXa:1XaXa:1XAY: 1XaY
x
Question: Why do genetic diseases "skip" generations when they're recessive? What are these diseases caused by?
Pear Deck Interactive Slide
Students, draw anywhere on this slide!
Do not remove this bar

Key Diseases: Mendelian & Non-Mendelian 3/25,26 Some More important Diseases and more about the ones on previous page Mendelian: Albinism, Sickle cell: AR Achondroplasia: AD (and what happens if 2 dominant alleles come together? Dead. Symptoms of Aa dwarf are that gait is abnormal, size is abnormal, physiology is abnormal. Hemophilia: XR: the intervention is an injection of the appropriate recombinant clotting factor. Notable Chromosome abnormalities: Diagnose with karyotype: What is a karyotype? Down: Trisomy 21 (prolific autosomal disorder) Klinefelter’s XXY: first discovered chromosome disorder Turner XO: only viable monosomy Y linked defects are rare. SRY sex reversal is an example. Chromosome balance: Normal males XY (44+XY) and Normal females XX (44 + XX) X inactivation needed for females: Y is extra stuff: Why and how do Barr Bodies form? What’s X inactivation? What is heterochromatin?

Key Diseases: Mendelian & Non-Mendelian 3/25,26
Some More important Diseases and more about the ones on previous page
Mendelian: Albinism, Sickle cell: AR
Achondroplasia: AD (and what happens if 2 dominant alleles come together? Dead. Symptoms of Aa dwarf are that
gait is abnormal, size is abnormal, physiology is abnormal.
Hemophilia: XR: the intervention is an injection of the appropriate recombinant clotting factor.
Notable Chromosome abnormalities: Diagnose with karyotype: What is a karyotype?
Down: Trisomy 21 (prolific autosomal disorder)
Klinefelter’s XXY: first discovered chromosome disorder
Turner XO: only viable monosomy
Y linked defects are rare. SRY sex reversal is an example.
Chromosome balance: Normal males XY (44+XY) and Normal females XX (44 + XX)
X inactivation needed for females: Y is extra stuff:
Why and how do Barr Bodies form? What’s X inactivation? What is heterochromatin?

Key Non-Mendelian Diseases: Mendelian 3/27 & important previous Some More Diseases and about the page more ones on Mendelian Diseases Chromosome Chromosome Balance Notable Abnormalities & X Inactivation Albinism, Sickle cell: AR What karyotype? is a (44+XY) fxr Normal males XY XY and (prolific Normal females (44 XX) Achondroplasia: (What AD. 821s Down: Trisomy 21 XX + happens 21st disorder) if alleles 2 dominant autosomal Ch together? Symptoms come Dead. of Aa dwarf are that gait is Klinefelter's XXY: first 8 X inactivation needed for abnormal, abnormal, size is XXY discovered chromosome females: Y is extra stuff: physiology abnormal.) is disorder Hemophilia: XR: the intervention Turner XO: only viable Why and how do XO Barr injection is of the an monosomy Bodies form? appropriate recombinant clotting factor. What's inactivation? Y linked defects SRY X are rare. is example. sex reversal What an is heterochromatin? Pear Deck Interactive Slide Students, draw anywhere this slide! on Do this not remove bar

Key Diseases: Mendelian Non-Mendelian 3/27
&
Some More important Diseases and about the previous page
more ones on
Mendelian Diseases Notable Chromosome Chromosome Balance
Abnormalities & X Inactivation
Albinism, Sickle cell: AR
What is a karyotype? (44+XY)
fxr Normal males XY
XY and
Achondroplasia: AD. (What 821s Down: Trisomy 21 (prolific Normal females XX (44 + XX)
happens if 2 dominant alleles 21st autosomal disorder)
Ch
come together? Dead. Symptoms
of Aa dwarf are that gait is Klinefelter's XXY: first
8 X inactivation needed for
abnormal, size is abnormal, XXY discovered chromosome
females: Y is extra stuff:
physiology is abnormal.) disorder
Hemophilia: XR: the intervention Turner XO: only viable Why and how do
XO Barr
is an injection of the
monosomy
Bodies form?
appropriate recombinant
clotting factor. Y linked defects SRY What's X inactivation?
are rare.
sex reversal is an example. What is heterochromatin?
Pear Deck Interactive Slide
Students, draw anywhere on this slide!
Do not remove this bar

More Atypical Inheritance: Epistasis & Non-Allelic Gene/Gene Product Interaction: finish by 3/26. (in h/o) Epistasis: multiple gene products contribute to a final outcome: best examples are when we do a dihybrid and don’t get the traditional 9:3:3:1: we get a modified form of this. Recessive epistasis is manifested as 9:3:4. Dominant epi manifests as 12:3:1. Complementary genes can manifest a few different ways but most famous one is from bateson-punnett study =>: 9:7 A different category than recessive at either or both. Each of these ratios emerges bc of the roles of A/a and B/b relative to one another. 9-3-4 you see in agouti mice , labrador retrievers, many flowers 12-3-1 you see in foxglove and snapdragons 9-7 you see in flowers (Bateson Punnett) You can see all of these in petunias! More complex sets of gene interactions can involve 5 or 6 loci. How can you imagine gene products interacting in a biochemical pathway?

More Atypical Inheritance: Epistasis & Non-Allelic
Gene/Gene Product Interaction: finish by 3/26. (in h/o)
Epistasis: multiple gene products contribute to a final outcome: best examples are when we do a dihybrid and
don’t get the traditional 9:3:3:1: we get a modified form of this. Recessive epistasis is manifested as 9:3:4.
Dominant epi manifests as 12:3:1. Complementary genes can manifest a few different ways but most famous
one is from bateson-punnett study =>: 9:7
A different category than recessive at either or both. Each of these ratios emerges bc of the roles of A/a and
B/b relative to one another.
9-3-4 you see in agouti mice , labrador retrievers, many flowers
12-3-1 you see in foxglove and snapdragons
9-7 you see in flowers (Bateson Punnett)
You can see all of these in petunias! More complex sets of gene interactions can involve 5 or 6 loci.
How can you imagine gene products interacting in a biochemical pathway?

Labrador retrievers (epistasis): E/e is epistatic to B/b From Wikipedia: What kind of inheritance is this and why? Why are The blonde dogs blonde? Below is the best explanation I have ever seen for the chart at right. https://mapleleafvet.com/genetics-of-labrador-coat-color/

Labrador retrievers (epistasis): E/e is epistatic to B/b
From Wikipedia:
What kind of inheritance
is this and why? Why are
The blonde dogs blonde?
Below is the best
explanation I have ever
seen for the chart
at right. https://mapleleafvet.com/genetics-of-labrador-coat-color/

(Epistasis): Epistatic B/b Labrador Retrievers E/e is to From Wikipedia: ee BbEe What kind of inheritance BE bE Be be is this and why? Why are BE BbEE BBEE BBEe BbEe 9 Black The dogs blonde blonde? B-E- bE BbEe bbEe bbEe BbEE BbEe bbE- BbEe Below is the best Chocolate BBee 3 bbE- ee Be BBEe BbEe BBEe bbee BbEe explanation I have ever Yellow lee 4 Dudley (bbee) 1 is for the chart be seen BBee bbEe BbEe bbee bbee bbee right. https://mapleleafvet.com/genetics-of-labrador-coat-color/ at Pear Deck Interactive Slide Students, draw anywhere this slide! on Do not this remove bar

Labrador Retrievers (Epistasis): E/e is Epistatic to B/b
From Wikipedia:
ee BbEe
What kind of inheritance
BE bE Be be
is this and why? Why are
BE
BBEE BbEE BBEe BbEe
The blonde dogs blonde? 9 B-E- Black
bE BbEE BbEe BbEe bbE- bbEe BbEe bbEe
Below is the best
BBee 3 Chocolate
bbE-
ee
Be BBEe BbEe BbEe BBEe bbee
explanation I have
ever
lee Yellow
4
1 is Dudley (bbee)
seen for the chart be
BBee BbEe bbEe bbee bbee bbee
at right. https://mapleleafvet.com/genetics-of-labrador-coat-color/
Pear Deck Interactive Slide
Students, draw anywhere this slide!
on Do not remove this bar

What to expect for 3 30 26 exam 20 questions All practical skills and crosses or cross analysis Practice the techniques and anything I told you to study Speed is important A classes have push ins 6th (after exam) and 8 (before exam).

What to expect for 3 30 26 exam
20 questions
All practical skills and crosses or cross analysis
Practice the techniques and anything I told you to study
Speed is important
A classes have push ins 6th (after exam) and 8 (before exam).

Faith Mtui - peardeckgenetics101sp26