Review Questions – Gametophytic Self-incompatibility (GSI)
Q.1
(10) Define gametophytic self-incompatibility (GSI). In grasses two loci are
involved in the manifestation of GSI and enhances the breeding efficiency. Consider
hypothetical loci to explain why the two-loci system in grasses is more efficient than the
single-locus system found in other species.
Q.2
(10) Describe the single-locus GSI system. What is the molecular basis of the
female determinant in a GSI system in Solanaceae?
Q.3
(15) Describe the female determinants of the GSI in Petunia inflata. How did Lee
and co-workers in 1994 prove the identity of the female determinant?
Q.4
(6 + 4) How can you prove that the RNase activity of the female determinant is
important for the GSI? Is there any natural mutant that may help you to address this
issue?
Q.5
(3 + 5) How is the allele-specificity of female determinants in GSI determined?
Provide experimental evidence to support your answer.
Q.6
(8 + 12) What are two hypotheses to explain the possible mechanism, by which
the GSI is manifested? Which one do you think is correct? Support your answer with
experimental evidence.
Q.7
(15) Do you think that there may be a male determinant in the GSI system?
Provide experimental evidence to support your answer.
Q.8
(25) Describe the role of aspargine-rich protein for the expression of S-allelespecific GSI in tobacco and tomato.
Q.9
(15) The female determinant in the GSI of field poppy is not an S-RNase. How
did Franklin-Tong group identify the female determinant of the GSI in field poppy? What
is the female determinant that they identified?
Review Questions - Sporophytic Self-Incompatibility (SSI)
Q.1
(5 + 5) Define sporophytic self-incompatibility (SSI). Describe the two classes of
S alleles.
Q.2
(5 + 5 + 5). Describe the three components of the SSI system.
Q.3
(12) Briefly describe the experimental evidence provided by Takasaki and coworkers in 2000 for the female determinant(s) of the SSI system.
Q.4
(15) Describe experimental evidence provided by either Schopfer and co-workers
(1999) or Takayama and co-workers (2000) for the male determinant of the SSI system.
Q.5
(3 + 3) Where do the male determinant genes in Class I and II type SSI alleles
transcribed?
Q.6
(15) What did you learn from the work reported by Shiba and co-workers in 2001
regarding expression of the male determinant protein? Describe the key result from their
paper with a suitable diagram.
Q.7
(20) Recently two independent groups have shown the direct interactions between
male and female determinants of the SSI system. Describe results from one of these two
groups to show the interaction between the two important components of the SSI system.
Q.8
(20) What are dominance and recessive in the manifestation of SSI? Describe
experimental results to explain the mechanism of dominance among male determinants.
Q.9
(15) How did Hatakeyama and co-workers show the mechanism of dominance
among female determinants in SSI?
Review Questions- Evolution of self-incompatibility:
Q.1
(5) What is the rationale for considering self-incompatibility as the driving force
for the rapid expansion of Angisoperms during the Cretaceous period by Whitehouse
(1950)?
Q.2
(4 + 3 + 3) What did Matton and coworkers (1994) conclude about evolution of
the self-incompatibility system in plants? What was the rationale for that conclusion?
Why did they speculate that gametophyte system was most likely evolved from the
sporophytic system by changing the time of expression of S locus in pollen from before
to after meiosis?
Q.3
(5 + 5) Describe the data presented by Igic and Kohn (2001), based on which they
concluded that GSI was the ancestral type self-incompatibility in plants. What were the
rationales for their conclusion?
Q.4
(10) Self-compatibility could be evolved through the mutation of selfincompatibility genes. Provide experimental data to support the above statement.
Review Questions-Evolution Of Polyploids
Q.1
(8) Literatures relating to evolution of polyploids have been greatly equivocal.
Describe a few earlier views about evolution of polyploids.
Q.2
(15) Describe the three classes of polyploids.
Q.3
(20) Discuss why polypolids are so successful.
Q.4
(10) Discuss the essential requirements for successful establishment of polyploids.
Q.5
(5) How is the genetic variation in polyploids generated?
Q.6
(20) It was earlier considered that duplicated genes in polyploids would be lost
due to deleterious mutations. Recent molecular data indicates that plant genomes carry a
higher percentage of duplicated alleles. Discuss why duplicated alleles stayed functional
over a long period following their duplication. Provide a suitable example to explain the
rationale for the survival of duplicated alleles (diagram should be considered).
Q.7
(15) Some gene combinations are deleterious or incompatible and could be deadly
for the survival of the newly formed polyploids. Describe how this problem is possibly
overcome following polyploidation.
Q.8
(15) Recent molecular data surprised our views about polyploids. Following
polyploidization newly united genomes go through a very active process of genome
reorganization. Substantiate the above statement with experimental data reported by Song
and co-workers in 1995.
Q.9
(10) Summarize the most important aspects that you have learned from the paper
by Ozkan et al.2001 on elimination of DNA sequences following polyploidization in
wheat?
Q. 10
(15) How did Shaked et al. (2001) study the possible epigenetic regulation of
DNA sequences following polyploidization in the wheat group? What were the outcomes
in their studies?
Q. 11
(15) How did Kashkush et al. (2002) study the alteration of gene expression
following polyploidization in wheat? What did they observed? Name the type of genes
that was only transcribed in the synthetic allotetraploids not in the progenitor plants.
Q. 12
(7) Does genome-rearrangement always take place following
polyploidization? Substantiate your answer with an example.
Q. 13
(10) What are the two hypotheses to explain the mode of action of the Ph1
gene in wheat? Describe briefly each hypothesis.
Q. 14
(20) How did the Moore group come to the conclusion that Ph1 plays an
important role in specific somatic and meiotic centromere association in wheat? Describe
the strategy they used and important findings they gathered in their studies.
Apomixis
Q.1
(10) What is the difference between obligate and facultative apomixis? Why is
evolution still possible in plants that reproduce through facultative apomixis?
Q.2
(15) What are two possible ways in which genetic diversity can be transferred
from diploid plants into polyploid plants?
Q.3
(10) What is the current theory used in explaining the genetic analysis of
Apomixis?
Q.4
(10) What are some of the things that make the genetic analysis of Apomixis
difficult?
Q.5
(10) Which are some of the potential advantages of the use of Apomixis in a Plant
Breeding program?
Q.6
(10) What are the controversies about the use of Apomixis regarding Biodiversity
and Genetic vulnerability?
Q.7
(10) Describe the two models, which explain the occurrence of apomixis.
Q.8
(10) Describe the enhancer detection technique.
Q.9
(20) What is apomixes? What are the types of apomixes? Why is apomixis
important in plant breeding? What are your views about the potentiality of apomixis in
developing F1 hybrids? Do you think that cloning of the gene(s) that regulates the
apomixis may attenuate some of the concerns that you may have for using apomixis in F1
seed production? If so, how the isolated gene(s) may help us to overcome your concern?
For the first quarter you may consider the questions of the first test (below).
First Exam:
Total 100
2/8/02
90 min
Part I:
Answer only 1 or 2, and 3
Total mark 30
1. What are the five most contentious issues reviewed by Fairbanks and Rytting (2001)? Which
one do you think to be the most important one and why?
15
2. What are the possible reasons for Mendel’s failure to report linkages?
15
3. Two of the traits studied by Mendel are now investigated at the molecular level. Based on the
results reported for one of these molecular studies on seed shape and stem length explain:
a. how a mutant phenotype is developed, and
10
b. how a wild-type gene functions as a dominant one, while a mutant gene as a
recessive one?
5
Part II
Answer one only
Total Mark 20
4. Draw the Synoptonomal complex and label its different parts. Where are the recombination
nodules (RN) detected? What is interference and what is the proposed model for the basis of
interference?
10+3+3+4= 20
5. Draw a ring bivalent of a pair of homologous chromosomes with their inner chromatids
exchanged through the crossing over event in both of their arms. Consider the gene order in
one chromosome is AAbbCCDD, while in the other homologous chromosome is aaBBccdd.
•
The centromere is located in between ‘B’ and and ‘C’ loci.
•
Assume that two crossovers occurred: one between A and B and the other between C and D.
Based on these information show the equational and reductional divisions for these loci at the
end of:
a) anaphase I, and
15
b) anaphase II.
Part III
5
Answer one only
Total Mark 20
6. You have just joined as a maize molecular geneticist position after completion of your
graduate studies. In your graduate studies you developed a high-resolution recombination
nodule map for the maze genome.
How will this knowledge help you in the current maize genomics position (which requires
mapping and cloning genes that govern traits of agronmic importance)? Justify your answers with
advantages that you will get from the maize RN map for identifying and isolating regions that
may carry your genes of interest.
7. What is an RN map? How do you develop it? Why is it a better cytogenetic map than a map
constructed based on the chiasmata? What are the possible reasons for the total genetic
distance in an RN map to be smaller than that in a molecular map?
5 x 4 = 20
Part III
Answer one only
Total Mark 30
8. As a graduate student you are to determine the inheritance of flower color in green beans.
Your major professor has provided with you the materials and data of the previous year to
investigate the issue.
-
He made several crosses using distantly related lines that carry either red or
white flowers.
-
He crossed a specific red flower carrying line only once with a specific line
carrying white flowers. He used four independent red flowering lines to cross
with four independent white flowering lines.
-
He thinks that red color is dominant over white and the flower color is
governed by a single gene.
-
The F2 segregations are shown below:
Cross
Red Flower
White Flower
I
77
25
II
60
40
III
80
27
IV
62
47
======================================
i)
What would be the null hypothesis to test major professor’s assumption?
Test the goodness-of-fit of these data and determine if this hypothesis is
correct. Are the segregation data heterogeneous? If so, explain the cause(s)
of variability among crosses.
15
ii)
Based on the results from the analysis in the previous step
develop your hypothesis to determine the number of genes
involved in the development of flower colors in green beans by
carrying out the goodness-of-fit test.
15