WELCOME GENETIC AND MOLECULAR BASIS OF

HETEROSIS NAME: YASIR ABBAS

12-ARID-332

INTRODUCTION HETEROSISHeterosis or hybrid vigour is the improved or increased function of any

biological quality in a hybrid offspring

GENETICAL BASIS FOR HETEROSIS.

MOLECULAR BASIS FOR HETEROSIS. QTL AND HETEROSIS.GENE EXPRESSION AND HETEROSIS.

EPIGENETIC BASIS FOR HETEROSIS.

QUANTITATIVE GENETICS OF HETEROSIS.

Refers to the phenomenon in which hybrid progeny of two inbred varieties

exhibits enhanced growth or agronomic performance.

Heterosis was first described by Charles Darwin (Darwin 1876) and

independently rediscovered by Shull (1908) and East(1908).

(‘‘I raised close together two large beds of self-fertilised and crossed seedlings

from the same plant of Linaria vulgaris. To my surprise, the crossed plants

when fully grown were plainly taller and more vigorous than the self-fertilized

ones.’’ - Charles Darwin )

Term coined by “SHULL” in (1952) as “ stimulation of heterozygosity”.

HETEROSIS

QUANTITATIVE DEFINITIONMID-PARENT HETEROSIS: It indicates that a trait displays hybrid performance that is significantly better than the average(mid-parent) valve.

BEST-PARENT HETEROSIS: Indicates that a hybrid trait performs significantly better than the better of two homozygous parents.AA BB AB(case1) AB(case2)

OffspringParents

Mid –parent heterosis

Best- parent heterosis

Performance

Best-parent

Mid-parentMid parent Heterosis (MH) = [ (F1- MP)/ MP ] x 100

Better parent (BP) = [ (F1- BP)/ BP ] x 100

GENETIC MODELS FOR HETEROSIS

Dominance

True/PseudoOver-dominance

Epistasis

DOMINANCE MODEL:

The dominance hypothesis explains heterosis by the complementing action of

superior dominant alleles from both parental inbred lines at multiple loci over the

corresponding unfavorable alleles, leading to improved vigor of hybrid plants

OVERDOMINANCE MODEL:

Over-dominance hypothesis attributes heterosis to allelic interactions at one or

multiple loci in hybrids that result in superior traits as compared to

•PSEUDO-OVERDOMINANCE:

The genetic intermediate of dominance and ODO IS Pseudo-ODO, which is actually a

case of simple dominance complementation, because of tight repulsion phase

linkage and appears to be ODO.

•EPISTASIS MODEL:

The epistasis hypothesis considers epistatic interactions between nonallelic genes at

two or more loci as the main factor for the superior phenotypic expression of a trait

in hybrids (Powers 1945).

Cancelling of deleterious

or inferior allells

Heterosis depend on

number of dominant

genes.

Both parents should

differ in dominant genes.

According to Panday

Complementation across

loci must be cumulative

to produce a superior

phenotype.

DISCUSSION ON DOMINANCE MODEL

AA CC EEbb aadd cc ddee BB*

Aa Cc EeBb dd

P1 P2

F1

Parent A

Parent B

Hybrid

AB

Quadrip

lex hyb

rid ABCD

Hybrid

CD

Parent C

0

1

2

3

4

5

6

7

Progressive heterosis refers to the fact that double cross hybrid autotetraploids (ABCD) typically show greater vigor than single cross hybrids (AABB; CCDD and so on). Increasingly superior alleles at any one locus must be added to the genotype with each different genome introduced in the tetraploid without contributing inferior alleles at other loci. The probability of this occurring is low. This observation argues against simple complementation as the sole basis of heterosis; therefore, there must be an additional molecular explanation.

PROGRESSIVE HETEROSIS

Parent D

DISCUSSION ON OVER-DOMINANCE• This model proposes that allelic

interactions at a single heterozygous locus result in a synergistic effect on vigor that surpasses both homozygous parents.

• No assumption of dominant- recessive relationship.

• Both alleles function together.• Single or small segment of genomes are

responsible for heterosis.• East (1936) postulated that divergence of

alleles brought together in heterozygotes, tend to increase the vigour of heterozygote.

*

P1 P2

A’ A

B” B”

F1

A’

A’

A

A

BB

BB”

A1A4>A1A3>A1A2------------- so on

OVER-DOMINANCE

EPISTASIS AS GENETIC MODEL FOR HETEROSIS

•

• Evidence that the interaction of favorable alleles at different loci

contributed by the two parents, which themselves may show additive,

dominant, or overdominant action

• The genetic background and allelic interactions therein can have an

effect on the heterotic contributions of individual loci.

QUANTITATIVE GENETICS OF HETEROSISClassical approaches of quantitative genetics to elucidate the genetic basis of heterosis

include :

1.Generation means or diallel analyses and

2.Estimates of variance components reflecting different types of genetic effects .

Comstock and Robinson (1952) used generation mean to estimate the average degree of

dominance, but it ignores the effects of epistasis in estimates of additive and dominance

variance components.

The triple testcross (TTC) design provides a test for contribution of epistasis to

heterosis.

MOLECULAR BASIS OF HETEROSIS

Genetic basis

of heterosis

were coined

before the

molecular

concepts of

genetics were

formulated and

are not directly

connected with

Molecular

principles.

AT MOLECULAR LEVEL TWO MODELS ARE USED TO EXPLAIN HETEROSIS.

One model considers that in hybrids having two different kinds of alleles an allelic expression in additive manner occurs

.

In the second model the combination of different alleles causes gene expression changes in hybrids that deviate relative to mid-parent.

QTL AND HETEROSIS

Molecular breeding may act one of the promising approach to un reveal genetic

basis of heterosis.

Mainly used to identify genes or genomic regions that contribute heterosis for trait

of interest, that may be used in MAS to increase performance of hybrids but still

challenging.

Numerous QTLs with different levels of dominant, over dominant, and epistatic

effects have been mapped for heterosis in Rice (Li et al., 2001;Luo et al. (2001),

and Mei et al. (2003, 2005),

CONCLUSIONS FROM THESE QTL AND MARKER BASED STUDIES.

The specifically detected QTL indicate that different factors are of relevance

under different conditions and it is difficult to decipher molecular basis using

only one hypothesis actually may be caused by combinations of these mutually

nonexclusive mechanisms

The complex trait ‘heterosis’ is expected to be reflected by many genes, their wide genomic distribution, the combination and interaction of which may depend on the organism and trait under study .

QTL may not always directly control an individual agronomic trait but may instead be regulatory in nature, mediated by multi subunit complexes, are dosage dependent that would contribute to the multigenic control of the ultimate phenotype .

There is variation in the relative level of heterosis for different traits between different hybrids. This variation suggests that the same set of genes does not control all heterotic responses.

A CAUSE OF HETEROSISEPIGENETICS AS

“Epigenetics” refers to heritable (through mitosis or meiosis) alterations in gene expression that are independent of DNA sequence: different epigenetically regulated forms of a gene are known as epialleles.Epigenetic information systems, could generate epigenetic variation/epiallels that had never been considered as the cause of phenotypic variation .

In addition, local chromatin status, mediated through epigeneticmodification, can potentially affect gene expression in cis (at the gene itself) or in trans (by regulating loci indirectly).

TYPES

DNA METHYLATION

HISTONEMODIFICATION

RNAINTERFERANCE

siRNAs, miRNAs etcCHROMATIN REMODLING

DNA METHYLATION AND HETEROSIS

DNA methylation is a biochemical process where a methyl

group is added to the cytosine or

adenine DNA nucleotides. Conversion of cytosine to 5 methyl cytosine.

DNA methylation does not change the DNA sequence and its function, but

does change its expression level, referred as an epigenetic change.

Associated with gene silencing, and genes with abundant 5-methylcytosine in

their promoter region are usually transcriptionally silent.

Basically heterosis is a result of ‘‘different alleles’’

being present at loci that contribute to the regulatory

hierarchies that control quantitative traits .

These ‘‘different alleles’’, however, can arise from

differently methylated DNA. If so, homozygosity of

methylated DNA in such regulatory factors suppresses

gene expression, while its heterozygosity regulates.

Heterosis in riceNational Key Laboratory of Crop Genetic Improvement

Experiment,

They use rice as the model system.

They make a cross between Zhenshan 97 and Minghui 63 to

derive an F2:3 population and an "immortalized" F2 population .

The hetrosis is due the involvement of large numbers of

two-locus interactions, or epistasis, underlying the genetic

basis of quantitative traits.But the contributions of the genetic

components varied with traits

Overdominance/pseudo-overdominance is the most important contributor to heterosis of yield, no. of grains/ panicle, and grain weight. Dominance × dominance interaction is important for heterosis of tillers per plant and grain weight and has roles in yield and grain number. Single-locus dominance has relatively small contributions in all of the traits. The RNA fragments were sequenced and mapped to the rice linkage map, which provided insights into the understanding. They analyses ,both combining genetic and molecular approaches will eventually lead to the characterization of the biological mechanisms of heterosis.

CONCLUSION

. Despite the use of advanced technologies it stillremains un clear what is the actual cause of heterosis.

However one common theme through out the century was that heterosis is complex issue, that is organism , population and trait dependent. Genetic and molecular approaches lead to the characterization of the biological mechanisms of heterosis

Thanks for patience listening