Download Review 16-18

 Review 16-18
 The search for the genetic material
involved many experiments
 Griffin-transformation
 Hershey/Chase –Sulfur/Phosphorus
 Franklin & Wilikins/Watson & Crick-double
helix w/bases in middle held together by
H-bonds
 Antiparallel
 Chargoff’s base-pairing rules-A/T & C/G
 Transformation-assimilation of external
DNA into a cell
DNA replication:
Begins @ origin of replication (bubbles)
Helicase- separates strands
Ss binding proteins stabalize strands
Leading strand is made by DNA pol adding
nt’s 1 by 1 in the 5’ to 3’ direction
 Primase attaches to other strand &
makes RNA primer for Okazaki
fragments
 DNA pol adds nt’s to the primer
fragment
 Ligase binds the fragments together
by covalent bonds
 DNA pol’s proofread nt’s & if 1 is
found to be wrong it takes it out &
replaces it
 Mistakes not caught right away are
cut out later by enzymes called
nucleases
 This is called nt excision repair
 Telomeres-nt seq’s at the ends of
chromosomes
 They protect DNA from being eroded
after many cycles of replication
 They protect the genes on the end of
chromosomes
 They get shorter w/each replication &
are shorter in older people’s cells
 Telomerase-lengthens the telomeres
in germ cells & compensates for the
shortening that occurs w/replication
 Not active in most somatic cells
 Germ cells give rise to gametes
 Ch 17
 From gene to protein
 DNA- A T C G; ds
 RNA- A U CG; ss
 Adenine is in DNA, RNA, & ATP
 1 gene 1 pp
 Txn-in the nucleus it is written from
DNA template
 mRNA processing-then the introns
are cut out & a cap & tail is added
 In the cytoplasm it is translated at the
ribosome into a pp
 Codons-3 letter words that code for
each aa during tsln
 Look at pg 314
 What is the possible seq of nt’s in the
template strand of DNA that would
code for the pp phe-leu-ile-ala-val?
 Aaa-gaa-taa-cga-caa
 What pp will be made from
 Aug-ucu-uca-uua-ucc-uuu?
 Met-ser-ser-leu-ser-phe
 Txn 3 stages
 Initiation, elongation, termination
 Initiation begins w/initiation complex
 A promoter region on DNA
 Including the TATA box ~25 nt’s
upstream from start point
 Txn factors bind to help RNA pol bind
 DNA strands unwind
 RNA pol transcribes mRNA
 Remember way back to cell
signaling?
 Txn factors can be signals from
hormones or other molecules
 Used to turn genes on or off by
blocking txn
 Elongation
 RNA pol moves downstream
unwinding DNA and elongating RNA
transcript in 5’→3’ direction
 Double helix reforms as RNA pol moves
on down the line
 Termination
 Eventually RNA is released and RNA
pol falls off
 Not yet completely understood what
mechanism causes this
 Modification of RNA B4 leaving
nucleus
 Introns (non-coding regions) are cut
out
 A polyA tail is added to 3’end & a cap
is added to 5’ end
 Evolutionary role of introns:
 Some have seq’s that control gene activity
 Some genes code for more than 1 pp
depending on which segments are treated
as exons during RNA processing
 This is alternative RNA splicing
 **The presence of introns allows
exons to be moved around more
easily (exon shuffling) making new
proteins w/new combinations of
functional domains
 Tsln also 3 parts:
 Initiation, elongation, temination
 The players: mRNA, tRNA,
aminoacyl-tRNA synthetase,
ribosomes
 Structure of tRNA
 aa at 1 end & anticodon on other end
 Anticodon is complemetary to codon
 The function of the ribosome in pp
synthesis is :
 To hold the mRNA & tRNA together,
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 catalyze the addition of aa’s form
tRNA’s to the pp chain,
 & to move the mRNA along & eject
tRNA during translocation
 initiation stage of tsln
 Brings together mRNA, tRNA
bearing the 1st aa of the pp, & 2
subunits of a ribosome
 The small ribosomal subunit binds
w/mRNA
 An aminoacyl-tRNA binds to the A site
 A peptide bonds forms b/w new aa &
pp
 tRNA translocates to P site
 tRNA leaves P site & P site is vacant
until another tRNA has given up their
aa
 Termination
 The final stage of tsln is termination
 the ribosome reaches a stop codon
in the mRNA
 The pp may undergo further
modification B4 it becomes a
functional protein
 A polyribosome is a group of
ribosomes the read a single mRNA at
the same time
 While it’s being made the pp will start
to fold & coil spontaneously
 But…b4 it can do it’s job some aa’s
made be modified by the addition of
sugars, lipids, phosphate groups,
etc….
 Sometimes the pp is cut into pieces
b4 it is functional
 If the pp is destined for the
endomembrane system or secretion
it’s marked by a signal peptide
 This targets the pp to the ER
 The signal peptide is recognized by
by SRP’s (signal-recognition particle)
 The signal is usually removed & then
the rest of the pp is finished
 If it is to be secretory protein it is
released into ER soln
 Mutations- point mutations are the
most common kind
 They are the change of 1 nt
 Substitutions usually missense
(codes for aa but not the right one)
 Nonsense mutation (point mutation
that codes for a stop codon where
there should not be one)
 Pro’s vs Euk’s
 Prok have circular DNA & so don’t
have telomeres & has only 1 origin of
replication
 Txn & tsln take place at the same
time in prok’s (prok’s have no
nucleus)
 Prok’s don’t have introns!
 Ch 18
 Viruses have a genome but can only
replicate w/in a host cell
 Viruses are obligate parasites b/c
they cannot reproduce outside of a
host cell
 Phages can have 2 types of life cycles
 lysogenic- viral DNA is replicated w/host
DNA
 Lytic cycle- (virulent phages) host is
destroyed after making many baby viruses
 Viral structure is a nucleic acid which
can by ss or ds DNA or RNA
 surrounded by capsid (protein shell)
 ** ONLY some viruses have a viral
envelope
 Viruses that use ssRNA & reverse
transcriptase are retroviruses
 Vaccines & nucleoside analogs
(interfers w/viral nucleic acid
synthesis) are the only effective
weapons against viruses
 Viroids are the simplest infectious
biological systems
 Prions are misfolded versions of
normal brain proteins
 Gene transfer & recombination in
bacteria
 Transformation-external DNA is
assimilated by a cell
 Transduction-DNA is transferred from
2 bacteria to another by a virus
 Transposition-A seq of DNA is moved
to alternate locations in the genome
 Conjugation-a group of F+ bacteria is
mixed w/group of F- bacteria (after
days all are F+)
 Also a plasmid is exchanged via a
pilus
 What is an operon?
 A promoter, operator, & the genes
they control
 They are all part of the DNA
 An operon can be turned off by a
repressor (protein) that binds to the
operator & blocks txn by blocking the
attachment of RNA pol
 The repressor is a product of a
regulatory gene (in this case called
trpR)
 Regulatory genes are always on at a
low rate
 An inducer inactivates the repressor
 What is a ligand?
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EXPLAIN replication in detail
EXPLAIN how a gene in a eukaryotic cell is
transcribed & translated to produce a
protein. Draw these processes & label RNA
Polymerase, pre-mRNA, mRNA, introns,
exons, spliceosome, ribosome, tRNA,
codon, anticodon
EXPLAIN what changes may occur to the
mRNA b4 it leaves the nucleus
EXPLAIN how the genetic material from 1
bacterial cell enters another via
transformation, transduction, or conjugation
 In fruit flies, the phenotype for eye color &
wing shape is determined by certain loci.
E indicates the dominant allele and e
indicates the recessive allele for eye color
and W is normal wings and w is vestigial
wings. The cross between a fruit fly with
wild-type eyes and vestigial wings & sepia
eyes with normal wings (wild-type) yielded
the following results for the F1 generation:

Wild-type
sepia/normal
wild-type/vestigial
sepia/vestigial
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 F1
100
0
0
0
 F2
52
16
23
9
 Determine the genotypes of the Parental (P) generation.
 Show a Punnett square cross of the P generation and
the F1 generation (to show the expected F2 results)
 Use the Chi-square test to determine your chi-square
value of the observed vs. expected ratios.
 How many degrees of freedom is there in this analysis?
 A virus is an infectious particle that
replicate using the metabolic machinery of
their bacterial, animal, or plant host. Viral
infections may destroy the host cell and
cause disease within the host organism.
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Describe the basic structure of a virus
Why are they not considered alive?
What is a prion?
How does a vaccine work?