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Results and
discussion
Results of inoculation of experimental material are summarised in
Table1
and Table2.
NP4, Timagalen and Sonalika showed very good infection to the embryos
and so also expression of the disease at the adult plant stage
(Table1).
Chinese Spring exhibited embryonic infection but the disease was not
expressed. Reaction of ditelosomic lines (Table
2) revealed that
susceptibility was determined by three genes present on the long arm
of chromosomes 2A, 3A and 6B.
The absence of any one of the genes resulted in resistance of the
embryo to the fungus strain used. Monosomic 2A, 3A and 6B
(Table
2) behaved
exactly like the disomic. Obviously, the genes are hernizygous
effective for susceptibility but nullisomic condition as caused in
ditelosomic lines imparted resistance. It can thus be suggested that
susceptibility of embryo infection in Chinese Spring against the
inoculum used was controlled by at least three genes hen-dzygous
effective to cause susceptibility but in nulli-condition resulted in
resistance of the embryo against the fungus.
This is for the first time that genes have been identified for
susceptibility of embryo to infection of the smut. Since disease has
not appeared in the adult plant, it is quite evident that the genes
for infection and expression of the disease are different. So far
this distinction has not been made.
In the present study all the aneuploid lines of Chinese Spring have
shown adult plant resistance (Table
2). Effect of
absence of a single gene at a time did not cause any smutted ear
heads. This study shows that inheritance of disease expression is
complex in Chinese Spring. It is, therefore, suggested that there may
be at least two or more genes (may be interacting) conditioning
resistance to disease expression. However, the exact picture can be
drawn by conventional genetic analysis.
Chinese Spring with respect to the Indian inoculum used was found to
be susceptible to infection but resistance to the expression of the
disease. This is in contrast to the reports from Poland (Heindch
1970) and Ireland (Dhitaphichit et al 1989) where it gets infected
and develops disease. Obviously, the races in India and Poland or
Ireland are expected to be different. Infection and expression of
disease are genetically governed and hence this differential
behaviour of Chinese Spring can be used to distinguish pathogenic
races. So far, pathogenic races are differentiated on the basis of
disease expression on differential cultivars.
Location of genes on specific chromosome arms for conferring
susceptibility at embryonic level should prove to be of use in
identifying other markers together with RFLP markers. Such a study
can be of great use to wheat breeders for incorporating resistance to
this disease which otherwise is difficult to deal with. In addition,
for other characters, Chinese Spring with a number of factors
determining resistance to the smut can also be more successfully used
in hybridization programme.
References
Agrawal RK, Rao MV and Joshi AB (1963) Inheritance of loose smut
resistance in an inter-varietal cross of Triticum aestivum L.
Ind J Genet and PI Breed 23 (2): 135-140.
Dhitaphichit P, Jones P and Keane EM (1989) Nuclear and cytoplasmic
gene control of resistance to loose smut (Ustilago tritici
(Pers.) Rostr.) in wheat (Triticum aestivum) Theor and AppI
Genet 78 (6): 897-903.
Heinrich J (1970) Studies of genetic resistance of wheat to loose
smut [Ustilago tritici (Pers.) Rostr]. Hodowla Roslin
Aklimatyzaeja i Nasiennictwo 14 (5): 393-404.
Mathur HC and Kohli SP (1963) Inheritance of resistance to loose smut
in Triticum aestivum. Ind J Genet and PI Breed 23 (3):
256-258.
Mortan DJ (1961) Trypan blue and boiling lactophenol for staining and
clearing barley tissues infected with Ustilago nuda.
Phytopathol 51: 27-29.
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