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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
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