Variation in submergence tolerance

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http://www.a2mediagroup.com/data/images/news/categories/riceplant.jpg

Linkage mapping (quantitative)

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intolerant tolerant

Fine-mapping

Finding the causative variant

Transgenic test

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Transgenic test

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Fig. 2B

Single-locus:

AA x BB

AB (F1)

AB x AB

AAABBABB

(F2)

25% 50% 25%

AA

ABBA

BB

AA ABBA

BB

“Effect of having a B”

1 locus, incomplete dominance

Two locilong chrom

short chrom

locus 1

locus 2

Two loci

A A

A A

long chrom

short chrom

locus 1

locus 2

Parent A

Two loci

A A

A A

long chrom

short chrom

locus 1

locus 2

Parent AB B

B B

long chrom

short chrom

locus 1

locus 2

Parent B

Two loci

AA/AA x BB/BBA A

A A

long chrom

short chrom

locus 1

locus 2

Parent AB B

B B

long chrom

short chrom

locus 1

locus 2

Parent B

Two loci

AA/AA x BB/BB

AB/AB (F1)

A A

A A

long chrom

short chrom

locus 1

locus 2

Parent AB B

B B

long chrom

short chrom

locus 1

locus 2

Parent B

Two loci

AA/AA x BB/BB

AB/AB (F1)

A A

A A

long chrom

short chrom

locus 1

locus 2

Parent AB B

B B

long chrom

short chrom

locus 1

locus 2

Parent B

Locus1/Locus 2

Two loci

AA/AA x BB/BB

AB/AB (F1)

A A

A A

long chrom

short chrom

locus 1

locus 2

Parent AB B

B B

long chrom

short chrom

locus 1

locus 2

Parent B

Locus1/Locus 2

AB/AB x AB/AB

(F2)16 possibilities

Two loci, incomplete dominance

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or BA

Two loci, incomplete dominance

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or BA

or BA

Two loci, incomplete dominance

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or BA

or BA

Two loci, incomplete dominanceHow many squares of the Punnett square are represented here?

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Effect of B at locus 2

Two loci, incomplete dominance

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Effect of B at locus 2

Two loci, incomplete dominance

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0 0.5 1.0 1.5

Phenotype

Two loci, incomplete dominance

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0 0.5 1.0 1.5

Phenotype

*

What is the genotype?A. AA/AAB. AB/AAC. BB/AAD. AA/AB

Two loci, incomplete dominance

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0 0.5 1.0 1.5

Phenotype

*

What is the genotype?A. AA/ABB. BB/ABC. AB/ABD. AA/BB

Two loci, incomplete dominance

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0 0.5 1.0 1.5

Phenotype

*

How many F2’s have this genotype?A. 1/16B. 2/16C. 3/16D. 4/16

Two loci, incomplete dominance

Two loci, incomplete dominance

Fig. 3.17

Notation is different, trait is qualitative; math is the same.

2-locus interaction

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http://www.projects.roslin.ac.uk/chickmap/organism.html

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Leghorn Junglefowl

Two loci

JJ/JJ x LL/LL

JL/JL (F1)

J J

J J

long chrom

short chrom

locus 1

locus 2

Parent JL L

L L

long chrom

short chrom

locus 1

locus 2

Parent L

Locus1/Locus 2

JL/JL x JL/JL

(F2)16 possibilities

2-locus interaction

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2-locus interaction

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2-locus interaction

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Effect of J at locus 2

2-locus interaction

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Effect of J at locus 2

Effect of variation at locus 2 depends on genotype at locus 1: non-additive

2-locus interaction

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Effect of J at locus 2

Effect of variation at locus 2 depends on genotype at locus 1: non-additive

For example: locus 1 is polymorphism in a transcription factor gene that affects protein binding affinity, locus 2 is in a binding site

2-locus interaction

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Effect of J at locus 2

Locus 2 is epistatic to locus 1: effects of locus 1 are masked in individuals with JJ or JL,LJ at locus 2

Locus 2 follows a dominance model: JJ and JL,LJ have the same phenotype, LL differs

“The dominant allele of locus 2 does the masking”

Other foibles in QTL mapping

Pathogenic yeast

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Pathogenic yeast

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How did YJM145 gain the ability to grow at body temperature?

A model quantitative trait

A model quantitative trait

Lab parent

A model quantitative trait

Lab parent Pathogenic parent

A model quantitative trait

Lab parent Pathogenic parent

100 progeny ≥ pathogenic parent

NO progeny as extreme as diploid hybrid

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NO progeny as extreme as diploid hybrid

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Lab parent Pathogenic parent

NO progeny as extreme as diploid hybrid

Diploid hybrid

Did the mapping…

Significant linkage to yeast chrom XIV and chrom XVI.

Did the fine-mapping…

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Did the fine-mapping…

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Which gene is causative?

Tested in hybrid diploids

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Lab

Pat

hoge

nic

Lab

Pat

hoge

nic

Tested in hybrid diploids

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Lab

Pat

hoge

nic

Lab

Pat

hoge

nic

Tested in hybrid diploids

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Lab

Pat

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Lab

Pat

hoge

nic

Tested in hybrid diploids

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Different in sequence

Lab

Pat

hoge

nic

Lab

Pat

hoge

nic

One mutant gene…

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From pathogenic strain

One mutant gene…

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From pathogenic strain

From lab strain

One mutant gene…

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From pathogenic strain

From lab strain

So diploid with this gene from the pathogenic strain grows BETTER at high T.

Two mutant genes…

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From pathogenic strain

From lab strain

Two mutant genes…

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From pathogenic strain

From lab strain

Again, diploid with this gene from the pathogenic strain grows BETTER at high T.

Three mutant genes

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From lab strain

Diploid with this gene from the pathogenic strain grows WORSE at high T!

From pathogenic strain

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Three mutant genes

From pathogenic strainFrom pathogenic strain

From pathogenic strain

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Three mutant genes

From pathogenic strainFrom pathogenic strain

From pathogenic strain

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Three mutant genes

From pathogenic strainFrom pathogenic strain

From pathogenic strain

Alleles from the same strain at

different genes/loci can have different

effects.

No common coding alleles across strains

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No common coding alleles across strains

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And no expression differences of >3-fold…

Three mutant genes in same “locus”

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Three mutant genes in same “locus”

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Three mutant genes

So why did 0/900 haploid progeny have a phenotype as extreme as the diploid

hybrid?

Lab parent Pathogenic parent

NO progeny as extreme as diploid hybrid

Diploid hybrid

Lab parent Pathogenic parent

NO progeny as extreme as diploid hybrid

Diploid hybrid

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Linked mutations of opposite effect

Path

Linked mutations of opposite effect

Path

Lab

Linked mutations of opposite effect

Path

Lab

Very unlikely

“Multiple linked loci”