Module 4 - Genetics (Passing on Information)

Question 1

Definition of Genetics

Answer 1

study of inherited variation

Genome = entire genetic complement of an organism (that is inherited)
Genes = functional units within a genome which is made up of nucleic acids (was originally all RNA but evolved to DNA as it is more stable for storage) (genes may or may not code for proteins)

Nuclear and extranuclear genomes = DNA found in nucleus and extranuclear DNA found in mitochondria and chloroplasts

Epigenetic states = how information in a genome is expressed

Question 2

Clonal Inheritance

Answer 2

where genetic material is copied (DNA replication) where copied material is accurately partitioned into daughter cells (horizontal transmission)
(horizontal transmission = movement of genetic information between unicellular or multicellular organisms compared to transmission of DNA from parent to offspring (vertical transmission)

Question 3

Cell Cycle (eukaryotes)

Answer 3

Interphase

• G1 = cell growth and prepares for DNA replication (organelle production)
• S phase = DNA is replicated and synthesized
• G2 phase = cell finishes replication and prepares for division

Metaphase (mitosis)

Checkpoints at each stage in interphase to ensure accuracy/precision of replication
Checkpoint at G1 = there are growth signals to ensure cell has grown enough and DNA is not damaged
Checkpoint at G2 = where cell must be large enough for cell division and DNA was fully replicated
Checkpoint at metaphase = to ensure chromosome-spindle assembly

Question 4

Chromosomes

Answer 4

Homologous chromosomes = maternal or paternal pair of chromosomes (share structural features, e.g. size, banding patterns, centromere positions, same genes at same loci BUT NOT NECESSARILY SAME ALLELES)

Chromatid = single strand of chromosome (1 DNA molecule in 1 chromatid)
Sister chromatids (homologous chromatids) = pair of chromosomes that are identical (either paternal or maternal)

Question 5

Mitosis

Answer 5

During interphase, DNA is loosely packed (two copies of it)

PROPHASE - DNA is tight coiled (supercoiled) to form chromosomes and spindle fibres (microtubules made from tubulin) form
spindle fibres attach to centrosomes at pole of cells + centromere of chromosomes

METAPHASE - Microtubules are attached to centromere of chromosomes where they align in the middle of cell
1 identical sister chromatid facing each pole

ANAPHASE - centromeres break apart due to spindles pulling them apart (sister chromatids break apart)

TELOPHASE - nuclear envelop reforms and spindle fibres break down, chromosomes uncoil (1 copy)

Cytokinesis - after nucleus divides, rest of cell divides (division of cytoplasm and organelles)

Question 6

Genomes and Ploidy

Answer 6

Genomes are all not the same size (not dependent on organisms size)

PLOIDY - number of copies of genome (n)
Haploid - single copy of genome (n)
Diploid - 2n
Triploid - 3n

Ploidy is not static, it can change depending on organism’s life cycle, somatic cells/gametes or evolution

Life cycle: Mold (fungus) is haploid for most of its life but are diploid during zygote development
Fern - it is haploid during germination that form gametes, when gametes join together they form mature fern (diploid)

Somatic cells (every cell type except reproductive cells) vs gametes: when eukaryotes are mostly diploid (2n) but form haploid cells (gametes) but fuse together to form diploid cells
Gametes cannot replicate themselves, only merge to form zygotes (2n, somatic cells)
Zygotes, somatic cells can replicate themselves

Evolution: wheat in ploidy is changed over time
originally, two species (wheat and wild grass) shared a chromatid which was then replicated forming a hybrid plant
Diploid wheat became hybrid which became tetraploid after replication
Tetraploid wheat mated with another species of wild grass having 3 chromatids of each species
After replication, the wheat became hexaploid (mitotic disjunction)

Question 7

Chromosome infos

Answer 7

Genetic material can be circular (prokaryotes) or linear
Substructures: centromere, telomere, origins of replication
Number of chromosomes ranges in different species (does not depend on genome size)

Genetic material is also found outside of nucleus in organelles (part of genome but exists outside)

PLASMIDS are extra individual genetic material (usually genetic advantages, e.g. antibiotic resistance)

Question 8

Genes and Alleles

Answer 8

Genes are present in almost all cells besides RBC (RBC have no genetic material as their sole function is transportation) (RBC do have information - mRNA - from original genetic material in order for proteins to function)

Genes in all cells are almost always the same besides in B cells (antibody producing cells)
-the produce specific antibodies by rearranging genes (different arrangement makes specific antibody to match antigen)

ALLELE - a copy of a gene that codes for different variations of a trait, alleles only differ by 1 or a few bases
-diploids have two copies of every gene, thus two alleles (can be identical or different)
Wild type allele - most common allele (mutant allele is other type)

Variance in genes are by:
-location on gene (loci), different possibilities/arrangement of bases, number of chromosome copies, different functions (due to variance)

(rRNA genes are duplicated in our body as we need many of them)

Question 9

Meiosis (vertical transmission)

Answer 9

-allows for genetic transmission and random assortment
(ploidy has to change during meiosis, as if it remained the same, number of chromosomes will always double)

Chromosomes halves in number during meiosis (n, 4 gametes)

PROPHASE 1 - supercoiling of chromosomes, replicated chromosomes pair up in their homologous pairs to form a bivalent (pair of mixed chromosomes; exchange of material) where crossing over occurs, spindle network of microtubules form and nuclear envelop breaks down

METAPHASE 1 - bivalents line up at the equator, centromere are attached to microtubules (where random assortment occurs)

ANAPHASE 1 - microtubules contract to pull homologous pairs break apart to opposite poles (centromeres DO NOT BREAK) (pair of chromosome in each cell)

TELOPHASE 1 - same as mitosis

PROPHASE 2 - same as mitosis

METAPHASE 2 - chromosomes line up at equator and centromeres are attached to microtubules

ANAPHASE 2 - centromeres break and chromatids pull apart in opposites poles

TELOPHASE 2 - four haploid cells are formed, spindle fibre network breaks down, nuclear envelope reforms and chromosomes uncoil

Genetic exchange results in new combinations of alleles (recombination = crossing over between chromosomes, occurs during prophase 1 of meiosis)

CHIASMA - when crossing over occurs between two non-sister chromatids forming a recombinant

Question 10

Errors in division of chromosomes

Answer 10

Non disjunction = where a pair of chromosomes do not split up, causing one gamete to have an extra set of chromosomes (3n, triploid) and one gamete having one less set of chromosomes

Aneuploidy - having abnormal number of chromosomes in a cell (45 or 47 chromosomes, instead of 46)

Trisomy of chromosome 21 = down syndrome (due to incorrect division in meiosis 1)

Question 11

Autosomes and Sex Chromosomes

Answer 11

Autosomes = set of chromosomes that are identical to each other (any set of chromosomes beside sex chromosome)

Sex Chromosomes = determines sex of organism
(sex chromosomes at meiosis act like a pair of homologous chromosomes; gender depends on father’s allele whether it is X or Y chromosome as female’s is always X)

Homogametic = autosomes, same sex chromosomes (e.g. female human, grasshopper, drosphilia)

Heterogametic = different sex chromosomes (e.g. male human, drosphilia, female birds) (chromosomes that have different morphology thus having two different gametes)

Question 12

Sex Determination

Answer 12

Sex Determination can be:
-Environmentally influenced
Sex in reptiles are determined by incubation of eggs
(lizards/alligators, higher temperature = male
turtles, higher temperature = female)

-Genetic
-Ploidy
Females (workers and queen) are diploid (fertilized eggs), males (drones) are haploid (unfertilised)

-Ratio of sex chromosomes to autosomes
Drosphilia (XY system): female = X/A = 1 ratio, male = X/A = 0.5 ratio
Grasshoppers (XO system): female = XX, male = XO

-Sex determining chromosomes/gene
Mammals = XY system, Y determines maleness
Birds = ZW system, male = ZZ, female = ZW

Question 13

Sex Determination - Non disjunction of sex chromosomes

Answer 13

TDF gene mutation where it appears on X chromosome instead of Y (X determines maleness)

Non disjunctions at meiosis can occur in syndromes
XO = turner syndrome
XXY = klinefelter syndrome

In drosphilia: ratio determines fertility as well
males = XO (sterile)
XY = fertile

Question 14

Genes on a chromosome

Answer 14

Genes on a chromosome can be transcribed into forming a polypeptide (genes can be facing different directions even if on the same strand)

Homozygous = the two copies of alleles of a gene are the same

Heterozygous = the two copies of alleles of a gene are different

Hemizygous = only one copy of a chromosome (human male = 1 copy of X chromosome, 1 copy of Y)

Question 15

Variations that are inherited

Answer 15

Phenotypic variations can be
Naturally occuring
Laboratory induced

Phenotypic variations can be
Monogenic - controlled by one gene
Polygenic - controlled by two or more genes

Phenotypic variations can be affected by the environment

Question 16

Genotypes and Phenotypes

Answer 16

Genotype - description of genetic composition of an organism
-can derive from 1 individual (mitotic) or from 2 parents (meiotic)

Phenotype - description of morphological, physical, behavioural properties of an organism due to its specific genotype and interaction with the environment

Question 17

Mendel’s First Law

Answer 17

Gregor Mendel - indentified the principles of inheritance (experimented with pea plants; Pisum sativum)

First law = ALLELES WILL ALWAYS SEGREGATE AWAY FROM EACH OTHER TO FORM GAMETES (individual segregation)

Experiment with pea plants (monohybrid cross; Dominant and recessive)
1 parent = round peas
1 parent = shrivelled peas
Both parents are PURE BREEDING (homozygous; both alleles at the locus controlling the characteristic are the same)
F1 (flial 1) = offspring were all round peas and heterozygous

F2 = 1:2:1 ratio of genotype
phenotypic ratio = 3:1
2 homozygous and 2 heterozygous offspring

Heterozygous pea plants demonstrated round phenotype (dominant)

To get the frequency of an allele pair:
Multiple the frequency of each gamete with each other

Question 18

Incomplete Dominance

Answer 18

-Monohybrid cross
Incomplete Dominance = heterozygous individidual blends both phenotypic characteristics of genotype (both alleles are dominant)

Seen with snapdragon flowers
Phenotype = flower colour
R = red, r = white
Rr organism = pink

Question 19

Codominance

Answer 19

-monohybrid
Codominance - phenotypic traits of each allele are simultaneously expressed

Seen in fowl feather colour
Phenotype = colour of feathers
B = black; b = white
Bb = fowl with black and white feathers

Question 20

Test Cross

Answer 20

the testing of an unknown genotypic individual with a known homozygous recessive individual

(recessive alleles will always be masked by dominant alleles thus the phenotypic characteristics of offspring can determine unknown parent’s genotype)

If unknown genotype was heterozygous, the genotypic ratio of offspring would be 1:1 (Tt;tt) and phenotype would be 1;1 also

If unknown genotype was homozygous
genotype = 1 combination
phenotype = 1 phenotype (dominant)

UNLIKED GENES GIVE 1;1;1;1 RATIO (expecting 4 characteristics)

LINKED GENES GIVE DIFFERENT RATIO

Question 21

Human Blood Groups

Answer 21

Example of codominant alleles + multiple alleles

Blood type is determined by the antigens present on RBC surface
Gene that determines antigen is located on I locus (3 alelles)

A blood type can be:
IaIa or IaIo
(A blood type rejects B type blood by clotting it up as the allele for B antigen is not present)

B blood type can be:
IbIb or IbIo
(B blood type rejects A type blood)

AB blood type is: IaIb
accepts all blood type

O blood type: IoIo
(rejects all blood type as neither A/B allele is present to make antigen)

To determine blood type:

• we see reaction of RBC with added antibody
• adding Anti-A antibody to blood type A will cause it to clump
• AB clumps to both Anti-A and Anti-B
• O does not clump to any

Question 22

Sex Linkage (sex-linked genes)

Answer 22

Gene controlling a characteristic is found on sex chromosome
(inheritance patterns will differ by sex)

Homogametic/Heterogametic sexes will differ in number of alleles
Homogametic = 2 alleles, can be hetero/homozygous
Heterogametic = carries 1 allele, HEMIZYGOUS at locus

COLOUR BLINDNESS (sex linked)
Using a pedigree, we can demonstrate the colour blindness trait and describe the genetics behind
Colour blindness is more predominant in males as the have only one X chromosome (only need 1 recessive allele to have colour blindness)
If females are heterozygous, they are CARRIERS

Question 23

Reciprocal Test

Answer 23

Determines whether a gene is sex linked

Seen in drosphilia eye colour
-A female pure breeding white eyed fly is crossed over with male pure breeding red eyed (reciprocal phenotype of original experiment)
X(w) = white eyes
X(w+) = red eyes

F1 females = all red eyes
males = white eyed
-shows gene is sex linked as in the original experiment (F1 = all had red eyes)

Question 24

Mendel’s Second Law

Answer 24

Alleles of different genes will ALWAYS assort independently from each other into gametes (due to random orientation in metaphase, assuming genes are NOT linked)

Question 25

Dihybrid Cross (two loci, dominant)

Answer 25

Seen with pea plants

Cross between yellow, round pea x green, shrivelled pea
Each trait is controlled by a different locus

F1: independent assortment of pure breeding parents (SSYY x ssyy)
the only offspring we get is SsYy (yellow, round)
(shows that green, wrinkle is recessive)

Gametes of offspring can be:
SY, Sy, sY, sy
(FOIL rule - first outside inside last)

F2: 9 possible genotypes
4 possible phenotypes (9;3;3;1 ratio) = unlinked genes

2^n = number of possible gametes
n = number of loci
(humans have 2 homologous chromosomes, thus assuming only 1 loci on each, 2^23 = 8,388,608 possible gametes)

Question 26

Linked Genes

Answer 26

Linked genes are where there are two alleles controlling characteristics found on different loci on the same chromosome

As combination is random, exchange of genetic information may not occur over the allele loci meaning parental combinations are more prominent (non-recombinants)

The maximum observable frequency of recombinants is 50%
With alleles that are very close together, crossing over rarely occurs thus the ratio of gametes is simply 1;1 (parental combinations)
If loci are further apart, this increases chance of crossing over

If crossing over does occur, the ratio of gametes is always 1;1;1;1

MAP DISTANCE = (number of recombinants gametes/total progeny) x 100
Units = mu (map units) or cm (centimorgan)
The genetic map distance is simple defined as 1 mu
(this formula can be used for loci that are close to each other)

With linked genes, the allelic arragenements can differ:
CIS LINKED = capital alleles are on the same homologous chromosomes
(AB - parental; aB/Ab = recombinants)

TRANS LINKED = capital/small case letters are on same homologous chromosome
(AB = recombinant)

Question 27

Single Nucleotide Polymorphisms (SNPs)

Answer 27

single base mutation from original genome

-can either be deletion or insertion

Question 28

Effects of mutations on genes

Answer 28

• No effect
• Reduced/loss of function
• gain another/altered function

Question 29

Genetic Variation (recessive/dominant genes)

Answer 29

One functional allele is sufficient to produce a wild type phenotype (most common)

At molecular level, with homozygous wild type, the produce of both alleles is a dominant allele thus the chance of getting wild type phenotype is 100%

With heterozygous, the gene has to only express 50% to get the wild type phenotype (recessive/mutant allele does not interfere with the function of wild type allele DEPENDING on the nature of mutation)

Question 30

Genetic Variation (Incomplete dominance)

Answer 30

Unlike dominant/recessive, one functional allele is not sufficient to produce wild type phenotype

Heterozygous has 50% chance of expressing wild type phenotype, however with incomplete dominant genes, this 50% is not enough to purely show wild type phenotype
Therefore, we get an intermediate (phenotypic trait of both alleles are combined)
Half of each gene’s product is being made throughout cell where the phenotype is ‘diluted’

Question 31

Genetic Variation (Codominant)

Answer 31

With codominant genes, each allele is sufficient to generate a phenotype

Heterozygous individuals has 50% gene product of the wild type allele where both alelles are functional

The % of gene product can vary though (as cells can vary in level of expression, depending on the conditions) like environment

Question 32

Sickle cell anaemia

Answer 32

CO DOMINANT GENE

Hb(a) = wild type haemoglobin (round RBC)
Hb(s) = sickle cell (mutant alelle)

Hb(a) gene produces glutamic acid (position 6 on gene, codon GAG (on copied strand)

Hb(s) = gene produces valine instead (codon GTG) (1 base subtitution)

With a heterozygous individual, the person will have both normal RBC and sickle cell (they are CARRIERS)
-in terms of morphology of RBC, DNA sequence and protein, it demonstrates co dominant phenotype

Question 33

Skin Colour

Answer 33

POLYGENIC INHERITANCE = a characteristic/trait that is controlled by 2 or more genes

Skin colour is a trait that is controlled by 5 genes (these genes control whether melanin is produced or not, giving rise to skin colour)

E.g. albinos are homozygous recessive in ALL the genes that produce the mRNA for a precursor of melanin
(gene produces a precursor that gets transformed into melanin)
Mutant gene produces the protein (precursor) but it is NON FUNCTIONAL (unable to form pigment)

Question 34

Epistasis

Answer 34

Epistatic gene = gene that controls the expression of another gene (gene masks the phenotypic trait of another gene)

Fungus conidial colour 
Wild type = green 
Mutants = yellow or white colour
(colour is produced by spores; spores arise from diploid cells undergoing meiosis to form haploid cells)
(as it is haploid, phenotype=genotype)
Green colour = yA+ OR wA+
Yellow colour = yA-
White colour = wA-

If we cross over every colour combination, the offspring phenotype always is green (in zygote, 2n)
-the gametes produced show different colours though (phenotype = genotype)

In the case of crossing over yellow x white (we have to consider two loci)
yA-wA+ x wA-yA+
(we are unsure of where mutation is)
Since we know green is dominant, the zygote offspring (2n) appears green as there is a wild type allele present at both loci
-when it becomes a haploid (gametes) the colour changes
offspring (F1) demonstrate a ratio of 1:2:1 (green:white:yellow)

Green = yA+wA+
Yellow = yA-wA+
White = yA+wA- AND yA-wA-
(how come yA-wA- comes to white?)

yellow phenotype arises due to mutation at Y loci and white phenotype arises due to mutation at W loci (mutations affect enzymes the contribute to colour)

Mutation at Y loci affects enzymes that converts yellow to green (causing fungi to stay yellow)

As seen here, white is epistatic to yellow (mutation at W loci causes lack of enzyme to transform white to yellow, thus remains white)

Question 35

Lethality

Answer 35

alleles that cause death (only when allele is homozygous)
-due to death of organism, the ratio of genotype and phenotype is altered

-In the case of mice
Two yellow mice were breeded (both heterozygous A(y)/A
The offspring showed brown and yellow mice
Ratio = 1:2 (brown:yellow), but it should be 1:2:1
Due to lethality of homozygous (A(y)) - ratio became 1:2

Question 36

Quantitative traits/characteristics

Answer 36

Where multiple genes and/or alleles influence the phenotypic trait

Different combinations of alleles can cause final outcome to be different (can be very small or large differences)

Quantitative traits do not matter on the number of contributing loci, but the size of phenotypic differences between genotype compared with the variation within genotypic classes
(in polygenic, ALL alleles contribute equally)

Question 37

Genetic Mutations

Answer 37

Mutations can be spontaneous or induced

• spontaneous = replication errors
• induced = action of mutagens (if not repaired, it will be passed onto offspring)
  e. g. gamma rays, UV light, x ray
  e. g. chemical mutagens (causing base analogues, intercalating (insertion), hydroxylating, alkylating, deaminating, oxidative agents)

(damage to DNA is not the mutation, only when failure to repair damage causes inheritance of mutation)

Base analogue (substance very similar to nucleic acid that can replace a base) can cause wrong base pairing (e.g. C on template strand where complimentary base is G but base A is present)
DNA polymerase would notice error and repair but there are 2 ways it can be repaired:
-the base on sense strand (replicated strand) is changed thus offspring will have normal DNA (no mutation)
-base on template strand is changed thus offspring will have mutated DNA

(mutations can occur anywhere in genome, not just genes)

Question 38

Consequences of mutations depend on different factors

Answer 38

-Location of mutation on genome (within functional units or not)
-Type of mutation (size and nature of mutation)
(base substitution, deletion, insertion, chromosomal arrangement)
-Somatic cells vs germ line cells
(somatic cells = small changes to ourselves that won’t be passed on
germ line cells = higher chance of being passed onto offspring)
-Effect of mutations can range from:
no effect –> lethality

Question 39

Effect of mutation on coding region of genes

Answer 39

• mutation may or may not affect the amino acid sequence of proteins (genetic code is degenerate)
• changes may/may not affect structure of proteins

SINGLE NUCLEOTIDE POLYMORPHISMS (SNPs)
Point mutations (4 different types) if they occur at coding regions of genes
-Base substituion
Can cause effects:
Silent = change of nucleotide but no change in required amino acid
Missense = change of nucleotide that lead to a change in required amino acid (none to complete loss of function, depending on function of amino acid in protein)
Nonsense = change of nucleotide leads to a termination codon (nonsense codon) (no protein is made, only 1 other amino acid is made (MET) OR depending on where nonsense codon occurs)

-Base deletion or insertion
Frameshift = loss or gain of nucleotide alters the reading frame (all the subsequent triplets after mutation is read differently)
(all amino acids after insertion/deletion is different which can cause complete loss of function, but depending on where mutation occured)

Question 40

Thalassaemia (mutation in B-globin)

Answer 40

Thalassaemia is a disorder to RBC
lots of mutations (in B-globin) that lead to thalassaemia but only 3 specific mutation causes clinical symptoms
(e.g. glutamic acid –> valine)

shows that even though amino acid was changed, it may not affect function of entire protein as the change in amino acid can be tolerated

Question 41

Effect of mutations in non-coding regions of genes

Answer 41

Can occur in non-transcribed regions or in transcribed regions but NOT translated

Changes may or may not affect time of gene expression, location of expression and level of expression
(mutation in non-coding regions can affect coding genes leading to more/less proteins made)

Insertions/Deletions (indels)
-can be large or small (1 base pair - hundreds of kilobase pairs)
-mutations can disrupt reading frame, disrupt gene expression/regulation, or can fuse genes together
E.g. Muscular dystrophy
-majority of this case arises from mutation in DMD gene (dystrophin gene) (found on X gene, on short arm)
2 types:
Becker muscular dystrophy (more mild) = deletion alleles (183bp and 195 bp long), multiples of 3
(since it is multiples of 3, reading frame is not altered)
-INFRAME MUTATION

Duchenne muscular dystrophy (severe) = deletion alleles (148bp and 173bp long), not multiples of 3
(reading frame is shifted where all triplets downstream will having their reading frame changed = frameshift mutation)
-OUT OF FRAME MUTATION

Question 42

Chromosomal Mutations

Answer 42

Chromosomal mutations include: large deletions, inversions, translocations
Chromosomal mutations are generally large, can disrupt gene expression, regulation or function, can fuse genes together

• Deletion
• Inversion = change of sequence of genes (depending on breakage, mutation may have no effect on function)
• Duplication/Deficiency = where chromosomal crossover did not occur at the same loci leading one chromosome to lose some genes = deficiency; one chromosome to gain extra replicate genes = duplicate

-Translocation = crossover of non-homologous chromosomes forming a HYBRID (parts of two chromosomes joined together; whole chromosomes may even be joined together)
Examples of chromosomes joining together: reciprocal translocation of t(9;22)(q34;q11)
BCR-ABL gene fusion where translocation between these two genes causes ABL gene to be unable to regulate/function due to BCR gene = myelogenous leukaemia

Question 43

Variable Number of Tandem Repeats (VNTRs)

Answer 43

Tandem repeats = short sequences in our genome that are tandemly repeated (copy number can change due to errors in crossing over or replication)

e.g. Trinucleotide repeats in coding regions (in Huntingtin gene, HTT)
Huntington’s Disease
in HTT gene, at exon 1 we have repeats of n(CAG) in which normal repeats = less than 26 repeats
(27-35 repeats = increases chance of repeats changing number which can cause a mutation in allele
36-39 repeats = huntington’s allele with mild effects
more than 40 repeats = HD allele)

Question 44

Genetic Mutational Screens

Answer 44

Genetic mutational screens identify which genes enhance the phenotype of a mutation
-geneticists induce mutations to identify which genes control traits/functions

e.g. Drosphilia - genetics of development
2 mutations from wild type:
Ultrabithorax = mutation in 1 gene caused 4 wings and 2 thorax (advantageous mutation thus they were able to survive)
Antennapedia = mutation caused antenna to be replaced by legs leading to bad sensitivity = disadvantageous

Genetics of development (discovered through mutational screens)
-gene expression relating to development are precisely controlled spatially and temporally
-clustered in the genome
-order of gene reflects order in body plan
HOX GENES = set of genes that specify regions of body plan of an embryo along head to feet axis (found in mammals too; ensure that body parts are developed in the right parts)

E.g. Schizosaccharomyces pombe (yeast experiment)
-we got an understanding of cell cycle control (through genetic screening)
various stages of cell cycle + necessary genes for checkpoints was discovered by mutational screens of S. pombe and S. cerevisiae
(this knowledge was able to be applied to all eukaryotes + larger eukaryotes)

We were able to use ‘model organisms’ to understand fundamental processes in all organisms is due to shared ancestry (share lots of genes)
-worms, yeast, flies and humans share a significant number of genes