GeneLab:eFly

Biol10005 Genetics and the Evolution of Life: Assignment

PART A

Part B will be completed in your tutorial of the w/c 9/9 Group A and the w/c 16/9 Group B
Please bring PART A to this tutorial for submission
Date

Day

Name

AM / PM

Student No

GROUP A / B

Seat

Demonstrator

PROCEDURE
Answers are to be typed. If you have trouble creating superscripts, these can be written in by hand. If
possible print double sided
a. My mutations are Black Body and Sepia Eye
b. You are required to perform a dihybrid cross using the two gene loci at which these mutations occur.
The other allele is wild type at each locus. In the space provided show the outline of the crosses you
will perform
P- Black Body, Sepia Eye Female * Wild Type Male
Then Cross the G1 to produce the G2
Wild Type Female* Wild type Male (G1*G1)

c.

Perform these crosses using eFly generating 1000 offspring for each cross you complete, and show
the outcome of the crosses in a table exported from the program below. (see the instruction
document) . All loci are autosomal so do not separate the frequency of each sex

Sepia eye Black Body*Wild type

Phenotype G1
Wild Type
No. of offspring

1000

Wild Type*Wild type G1*G1

Phenotype G2
Wild Type
No. of offspring

550

Sepia eye, wild

type
0

Black body wild

type
0

Sepia eye,
black body
0

Sepia eye, wild

type
186

Black body wild

type
195

Sepia eye,
black body
69

Which is the dominant phenotype at each locus? Explain how you reached this conclusion.
The dominant phenotype is the wild type for both loci, as crossing a purebreeding wild type with a pure
breeding sepia eye black body, produced on wild type offspring and as this is a autosomal gene, it means
that wild type must be the dominant phenotype. And by crossing the G1 a ration of 9:3:3:1 was produced

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e. Choose allelic symbols for the two loci you have investigated. Type these in the space below (refer to
Practical 2 in the Laboratory Workbook and read the section on allelic notation in Drosophila).
+

Locus 1: (Wild type) b , (sepia eye) b

Locus 2: (wild type) s , (Sepia Eye) s

f. Using your allelic symbols (from above) show the genotypes and phenotypes of the flies for all crosses
in the dihybrid cross.
+

G1: Wild Type all b b s s

G2: 9 Wild Type: 3 Sepia eye Wild Type: 3 Black body Wild Type: 1 Black body Sepia eye
+
+
+ + +
+
+ +
+ +
+
+
+ + + +
4 b b s s: 2 b b s s : 2 b b s s : 2 b b ss: 2 b b ss: 2 bb s s: b b s s : bb ss
g. In the study of human genetic disease, model organisms are used. You have been assigned a model
organism. Think about why they are used and what would make a good model organism for the study of
human genetic disease. Locate the Subject Guide link on the LMS.
Using the Web of Science data base your task is to find a journal article that links studies in this
organism to a study of cancer. The article should have been published in the last five years.
When you locate the article cut and paste the Title, Author, Source and Abstract into the space
below. Read the abstract and find clues why this organism was used as a model organism.
Look below the abstract for KEYWORDS and list two other keywords that would lead you to this
article.
Copy-number variation of cancer-gene orthologs is sufficient to induce cancer-like sympoms in
saccharomyces cerevisiae
[1]

Author(s): de Clare, M (de Clare, Michaela); Oliver, SG (Oliver, Stephen G.)

Source: BMC BIOLOGY Volume: 11 Article Number: 24 DOI: 10.1186/1741-7007-11-24 Published: MAR 25
2013

Abstract : Background: Copy-number variation (CNV), rather than complete loss of gene function, is increasingly
implicated in human disease. Moreover, gene dosage is recognised as important in tumourigenesis, and there is an
increasing realisation that CNVs may not be just symptomatic of the cancerous state but may, in fact, be causative.
However, the identification of CNV-related phenotypes for mammalian genes is a slow process, due to the technical
difficulty of constructing deletion mutants. Using the genome-wide deletion library for the model eukaryote,
Saccharomyces cerevisiae, we have identified genes (termed haploproficient, HP) which, when one copy is deleted from
a diploid cell, result in an increased rate of proliferation. Since haploproficiency under nutrient-sufficient conditions is a
novel phenotype, we sought here to characterise a subset of the yeast haploproficient genes which seem particularly
relevant to human cancers.
Results: We show that, for a subset of HP genes, heterozygous deletion is sufficient to cause aberrant cell cycling and
altered rates of apoptosis, phenotypes associated with cancer in mammalian cells. A majority of these yeast genes are
the orthologs of mammalian cancer genes, and hence our studies suggest that CNV of these oncogenic orthologs may
be sufficient to lead to tumourigenesis in human cells. Moreover, where not already implicated, this cluster of cancer-like
phenotypes in this model eukaryote may be predictive of the involvement in cancer of the mammalian orthologs of
these yeast HP genes. Using the yeastset as a model, we show that the response to a range of anti-cancer drugs is
strongly dependent on gene dosage, such that intermediate concentrations of the drugs can actually increase a mutant's
growth rate.
Conclusions: The exploitation of data on the phenotypic impact of heterozygosis in Saccharomyces cerevisiae has
permitted the prediction of CNVs affecting tumourigenesis in humans. Our yeast data also suggest that the identification
of CNVs in tumour cells may assist both the selection of anti-cancer drugs and the dosages at which they should be
administered if they are to be a beneficial, rather than a deleterious, therapy.

Yeast has been used for a model organism in the circumstance, as the yeast has a similar gene set to
humans in relevance to haploproficiency, it is easily cultivated, and has a short life cycle while its very easy
to use the genome wide deletion library in yeasts to synthesize the effects of the deletion mutations that are
observed in humans to recreate the effect of cancers in yeast.

Keyword: 1 Copy number variation Keyword: 2 Haploinsufficiency