4.

1: Introduction to DNA
EQ: How do we know that DNA is the source of heritable information and what is the structure of DNA?
----The first part of the lecture explains how we know DNA is the source of heritable information. It walks you through a
series of experiments for which you need to understand the significance.
● Understand what a chromosome is
● Know the significance of Frederick Griffith’s experiment (transformation) - what does his experiment prove?
● Know the significance of the Hershey Chase experiment
○ Need to know that a bacteriophage has two parts (DNA and protein) to understand the experiment
----NOW: We know that DNA is the source of heritable information. The next section of the lecture will go into the
structure of DNA
● Know Chargaff’s rules
○ Why is it significant that these rules transcend across all species?
● Know the contribution of Watson, Crick, Wilkins and Franklin
● Be able to explain the structure of DNA
○ Sugar-phosphate backbone
○ Bases (Chargaff’s rules of pairing)
○ Double-helix

4.2: The Central Dogma

EQ: How do the instructions encoded in DNA yield a protein?
-----Now that we understand the structure of DNA, it is time to learn how it functions (how it carries heritable
information which become proteins we can see and use).
● Step 1: DNA Replication
○ The goal of DNA replication is to create additional, identical double-stranded DNA molecules.
○ Understand how DNA replicates semi-conservatively (one strand is the template (old) and another strand is
created (new)) = semi (half) conserved (saved)
■ Initiation
● Know the significance of the origin
● Know the significance of each of the four enzymes (DNA polymerase, helicase, primase and
topoisomerase)
● Know the direction of replication (read 3’ to 5’, created 5’ to 3’)
● Each strand is antiparallel so they are read in opposite directions
■ Elongation
● Understand the issue of antiparallel with the replication bubble
○ Leading strand and lagging strand (Okazaki fragments)
■ Termination
● DNA replication ends when entire strand has been copied
● Understand the significance of telomeres
● Understand proofreading as a mechanism to reduce mutation rate
● Step 2: Transcription
○ The goal of transcription is to create a single-stranded RNA molecule (mRNA) that can carry the information of
DNA out of the nucleus and to the ribosomes.
■ Initiation
● Understand the role of RNA polymerase
● Understand what a promoter is (usually a characteristic DNA sequence signalling where
transcription should start = TATATA)
● Know how this is process is similar and different between eukaryotes and prokaryotes -
hypothesize the significance of the similarities and differences
■ Elongation
● RNA is produced 5’ - 3’ (by reading DNA from 3’ to 5’)
● Only one strand is made - so no lagging strand
■ Termination
● Transcription ends at the end of a transcription unit.
● Step 2.5: Post-Transcriptional RNA Processing (eukaryotes only)
○ Understand the significance of the 5’ cap and the poly-A tail
 ■ Why is this only useful for eukaryotes?
○ Exon splicing (removing introns) - not much is currently known about introns and why we have them.
● Step 3: Translation
○ The goal of translation is to create protein from mRNA (which is carrying the instructions from DNA)
○ Understand the structure of the ribosome (A site, P site and E site)
○ Understand the basic role and structure of tRNA (bringing amino acids! - specificity!)
○ Know what a codon is
■ Looking at the codon chart (which will be given to you) notice there are 64 codons but only 20 amino
acids which means there is redundancy - why might this be significant?
■ Know that the codon chart is the same for all life - why is this significant?
○ Initiation
■ Start codon (AUG) begins translation - which means Met is the first amino acid always
■ Understand the role of anticodons on tRNA in binding to mRNA
○ Elongation
■ Understand how the mRNA moves through the ribosome so more codons can be “read”
■ Understand how tRNA’s use their anticodons to “read” the mRNA
■ Understand that tRNA are specific and will only get another of the same amino acid (once they have
“dropped off” their amino acid)
● Why is this specificity so important?
■ Understand that as amino acids are being added we are creating peptide bonds between them =
primary structure of a protein!
○ Termination
■ Stop codon
● Mutations
○ Know the different types of mutations and how they may affect a protein
○ Know that mutations happen in DNA

4.3: Mitosis
EQ: How can one cell divide into two identical copies of itself and why is this necessary?
● Understand why mitosis is necessary
● Understand the phases of the cell cycle: G1, S, G2 and M, as well as G0
● Get the vocab first:
○ Know the difference between chromosomes and chromatids
○ Know the difference between haploid and diploid
○ Know when the cell is haploid and when the cell is diploid in the various phases of the cell cycle
● DO NOT MEMORIZE THE INDIVIDUAL PHASES OF MITOSIS!!!!!!!!!!!! You do not need to know these!
● Know the overall flow from one cell to two cells - be able to explain how many chromosomes and chromatids are at each
stage

4.4: Cell Cycle Control

EQ: How is the cell cycle (mitosis) controlled and what happens if these controls fail?
● Know the function of checkpoints (overall) and know what the G1 checkpoint does
● What controls the checkpoint? Internal and external cues!
○ Internal cues: CdK, cyclin and MPF (know the function of each and how the concentration cyclin and MPF would
affect the checkpoint)
○ External cues: proteins created by OTHER cells or environmental cues (overcrowding, etc)
● Cancer = uncontrolled cell division
○ Mutations happen and there are genes that are present to make sure mutated cells don’t divide - this is what
checkpoint is for!
○ These genes, the ones that make sure mutated cells don’t divide, are called proto-oncogenes and
tumor-suppressor genes
■ Proto-oncogenes: stimulate cell division (gas pedal)
■ Tumor-suppressor genes: slow down cell division (brake pedal)
○ But what happens if the proto-oncogenes and tumor-suppressor genes are mutated
 ■ Mutated proto-oncogene = oncogene = always on (always gas)
■ Mutated tumor-suporessor gene = always off (never brake)

4.5: Meiosis
EQ: Where does variation in a population come from?
● The difference between asexual and sexual reproduction (both in mechanism and variability)
● Understand the basics of fertilization (haploid + haploid = diploid)
○ These haploid cells are called gametes (aka: sperm and egg)
Meiosis is the process of making these haploid cells!
● Know the difference between sister chromatids and homologous chromosomes (this vocabulary is very challenging, but
it is imperative that you know it before understanding meiosis)
○ Homologous pair = a pair of chromosomes (one from mom and one from dad)
○ Sister chromatids = identical copies of each chromosome (mom and dad) made during S phase
○ There are two sets of non-sister chromatids in one homologous pair. There are also two sets of sister
chromatids in one homologous pair. Did that make sense?
● Understand the simple diagram of meiosis
○ Know the difference between Meiosis I and Meiosis II (remember meiosis just means division)
○ Know there is no DNA replication between meiosis I and meiosis II
■ Why not? What are we trying to make?
● You do not need to know every phase of meiosis. However, you do need to know a couple of key points:
○ Crossing over: when non-sister chromatids in a homologous pair exchange information from the same gene
■ What is the point?
■ Happens in meiosis I
○ Independent assortment:Alignment of homologous pairs during meiosis I where each homologous pair lines up
independently of the other homologous pairs (i.e. its not like all “mom” chromosomes on the left and all “dad”
chromosomes on the right)
■ What is the point?
● Sexual reproduction is challenging (requires a mate - which requires energy) - wouldn’t think it would be evolutionarily
advantageous over time. However...it is! WHY?
● Understand what a karyotype is.
○ Know the difference between autosomes and sex chromosomes
4.6: Introduction to Mendelian Genetics
EQ: How are traits inherited and expressed?
● You don’t need to know about Mendel - however you should study his experimental design (e.g. why the peas were
chosen, what his control was, etc) because AP likes you to design your own experiments. It is helpful to look at a pristine
example :)
● Know this vocab:
○ True breeding
○ F1, F2
○ Cross
○ Wild-type
○ Monohybrid
○ Dihybrid
● Know what an allele is (know that a homologous pair has two alleles; sister chromatids are copies of the same allele)
○ Understand the difference between dominant and recessive alleles
■ Dominance does NOT mean more evolutionarily advantageous - it just means it will appear in a
heterozygous situation
■ Dominance is predetermined and constant
● Revisit genotype versus phenotype
○ Know homozygous and heterozygous
● Know Mendel’s laws:
○ Law of segregation: alleles segregate during meiosis randomly into gametes (each gamete inherits only one
allele)
○ Law of independent assortment: Alleles are inherited independently of one another (it is not like you will inherit
all of mom’s alleles or all of dad’s alleles - it is a combo!)
■ This is due to independent assortment during meiosis!
● Look at how to solve the genetics problems as we will be doing this in class!
● Know what a testcross is and why it is useful

4.7: Extensions to Mendelian Genetics

Same EQ as above - just know that Mendel got us understanding how traits are inherited/expressed, but since his research we
have found some exceptions. This does not mean Mendel’s laws are incorrect (actually, quite the contrary). It’s just that we have
added additional rules and understanding. The beauty of science - it is always changing and getting better with new brains (like
yours!)
● Understand the following term and how they are different from Mendel’s understanding
○ Incomplete dominance
○ Codominance
○ Multiple alleles
○ Polygenic inheritance
● What is the benefit of these different types of inheritance patterns?
● Understand linked genes (this is important!!!!!)
○ Linked genes are genes located on the same chromosome (and therefore the same allele)
■ These genes will not separate except during crossing over!!
■ The closer the genes are to each other on an allele, the higher the likelihood they will be inherited
together (the less likely they will separate during crossing over)
● Gene mapping
○ Sex-linkage example (recessive alleles carried on the x-chromosome) --- ignore the sexist graphic please :)
● You don’t need to understand the other examples, per se (however they are WILDLY interesting)
● You do need to understand that there are many exceptions to Mendel’s rules and this is only to increase variation (think
evolution!)

4.8: Human Genetic Conditions

EQ: What is the relationship between inheritance of traits and their effect on human health?
● Understand the basics of a pedigree - we will be practicing these in class
● Understand the difference between dominant and recessive conditions
○ Explain how the expression in phenotype varies between the two
 ○ Would it differ if a recessive condition was on the x-chromosome?
● Know x-linked dominant versus x-linked recessive conditions
○ How does the probability of expression vary between men and women in each?
● Know y-linked conditions
○ Always dominant (why?)
○ Very uncommon (why?)

4.9: Regulation of Gene Expression

EQ: How is gene expression controlled?
This is a great final lesson as it forces us to review the concepts from the central dogma!
PROKARYOTES:
● Prokaryotes regulate gene expression simply by not transcribing those genes (stop transcription = stop translation = no
proteins from the gene are made!)
● Operons = a cluster of genes that all contribute to one metabolic task
○ It is more efficient to turn on/off an operon as opposed to each individual gene
● Understand the difference between inducible and repressible operons
○ Inducible = always off, can be induced (or turned on)
○ Repressible = always on, can be repressed (or turned off)
● Know the lac operon as the model example of an inducible operon (know the mechanism of how it works exactly)
○ The lac operon is a set of genes that breakdown lactose
■ If lactose is absent, the operon is off
■ If lactose is present, the operon is on
■ The lac operon is always off, unless lactose is present
○ A repressor is always bound to the operator (where RNA polymerase would attach)
○ When lactose is present, it binds to the repressor (as allolactose) and its allosteric site thereby changing its
shape so it cannot bind to the operator.
■ This allows RNA polymerase to transcribe the genes necessary to digest lactose
○ What happens to lactose when the genes are transcribed?
■ What, eventually, happens to allolactose?
■ What, eventually, happens to the repressor?
■ What, eventually, happens to the operon?
○ NEGATIVE FEEDBACK...homeostasis!
● Know the trp operon as the model example of an repressible operon (know the mechanism of how it works exactly)
○ The trp operon is a set of genes that produce tryptophan (when tryptophan is absent)
■ If tryptophan is absent = the operon is on or off?
■ If tryptophan is present = the operon is on or off?
■ Trp operon is usually on to make tryptophan
○ When tryptophan is present it acts as a co-repressor, activating the repressor so it can bind to the operator
(tryptophan binds to the repressor allosteric site changing it to an active form)
■ The operator becomes active and can bind to the operator, thereby inhibiting RNA polymerase from
transcribing the genes that synthesize synthetic tryptophan (don’t need it if there is real tryptophan!)
○ Tryptophan is needed by the cell
■ What will happen to it over time?
■ What will happen to the co-repressor? What about the repressor?
■ What about the operator and the entire operon?
● AGAIN - negative feedback (Homeostasis!)
● Understand the CAP/cAMP operon as an example of “upregulation”
EUKARYOTES:
● Eukaryotes can regulate gene expression at every step of central dogma (pre-transcription, transcription,
post-transcriptional, translation, etc)
● DNA access
○ Histone proteins wrap chromosomes into tight, compact structures.
○ Only accessible DNA will be transcribed.
○ The way that histone proteins wrap chromosomes is heritable!
● Pre-transcription
 ○ In order for transcription to happen, certain transcription factors need to be present. No transcription factors at
the promoter (TATA box), then no transcription
○ This is the key mechanism by which cells become differentiated
■ All of your cells have 100% of your DNA, but not all the DNA gets expressed (it depends on the
transcription factors - which get separated during mitosis of embryo)
● Post-transcription
○ Alternative splicing (introns/exons)
● Pre-translation
○ Honestly - not truly understood. Don’t worry about this one - just know it exists.
● Post-translation
○ Unneeded proteins are discarded
● Overall - know that eukaryotes can regulate gene regulation using more methods than prokaryotes

4.10: Biotechnology & Viruses

EQ: What are ways that DNA can be manipulated?
EQ: How do viruses replicate their own genetic material?
● Biotechnology:
○ know the basics (simple, simple basics) of each technique and know the difference between genetic testing and
genetic engineering.
● Viruses
○ Know that a virus is an obligate intracellular parasite consisting of two parts (genetic information + protein coat)
○ Know what a phage is
■ Know the difference between lytic and lysogenic reproductive cycles
○ Know that eukaryotic viruses can either have RNA or DNA as genetic material
■ Understand the difference in how each is replicated in the host - which has more potential for
error/mutation?
○ Understand the advantage to mutation for viruses