Sorghum Diseases in India

was named Colletotrichum sublineola.
Mohamed Ali: I would appreciate if Dr
Mughogho will give me the name of the reference
for this correction.
Mughogho: The information can be found in
Sutton, B.C. 1980. Coelomycetes. Commonwealth
Mycological Institute, Kew, UK.
Mukuru: You mentioned that the antidote increases
downy mildew infection in a DM-susceptible
cultivar. Have you used the antidote on
a resistant cultivar? If so, what is the reaction?
Craig: The herbicide antidote Concep II ® does
not increase downy mildew severity in a resistant
cultivar.
El Hilu Omer: What is the name of the herbicide
associated with increased disease incidence and
how does it bring about increased incidence? Is
it through increased susceptibility of the host or
enhanced spore germination?
Craig: It is not a herbicide, but a herbicide antidote
named Concep II ® . Apparently the increased
disease incidence is caused by inhibition
of maturation of host tissue. The chemical has no
effect on spore germination of the pathogen.
de Milliano: Does Concep II® increase severity
of disease both for oospores and conidia?
Craig: Yes!
Duncan: Have you had an opportunity to work
with herbicide-resistant plants in relation to
downy mildew incidence in order to circumvent
the herbicide-antidote problem? Are you going
to research this area in the future?
Craig: No, I have not worked with herbicideresistant
plants, and do not plan to do this in the
future.
Vidyabhushanam: How do you explain the occurrence
of susceptible F2 plants in a cross between
two resistant parents, i.e., SC 414-14 x QL
3? Downy mildew resistance has been reported
as dominant in both the parents.
Craig: The susceptible phenotypes in the F2 gen­
eration occur because the loci of the resistant
factors in QL 3 differ from the locus of the resistant
factor in SC 414-12.
Balasubramanian: The types of resistance to
downy mildew—is one to oospore and the other
to conidia?
Craig: Not to my knowledge. I have seen no case
in which cultivars resistant to conidia were susceptible
to oospores. Because of our inability to
get consistent infection using oospore inoculum
in the greenhouse, I have not been able to test
the reverse possibility.
Andrews: You said that a nondominant complex
of minor genes would offer the best type of genetic
resistance. How feasible do you think this
would be to breed for? It might be possible in
varieties— but wouldn't it be very difficult for
hybrids, where the resistance has to be incorporated
in both parents?
Craig: Generally it would be difficult. It would
involve going back and generating a new germplasm
pool with diversity of resistance and then
select, avoiding major gene resistance.
Laing: Have you tried propamocarb (Previcar
N ® ) from Scheming on sorghum downy mildew?
Craig: Dr Odvody has told us that propamocarb
did not work in his downy mildew trials when
applied as a drench.
Nowell: A comment on horizontal resistance
(HR). We have found that gains in HR are
equally quick in composites and in pedigree
breeding, or gene-stacking as it is sometimes
called. Possibly the most important factor is the
genetic diversity of the material that is initially
used to create the source material.
Craig: Yes, this is true. Our difficulty with minor
genes for controlling downy mildew is in recognizing
these minor factors. I have not devised a
method for identifying these factors.
Putter: In reply to a previous question, you explained
that you do not have a selection criterion
that will reveal what you call polygenic,
minor gene resistance. You also explained that
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