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AU / OTHER / BIOL / what is Eukaryotic Replication?

what is Eukaryotic Replication?

what is Eukaryotic Replication?

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School: Auburn University
Department: OTHER
Course: GENETICS
Term: Summer 2019
Tags:
Cost: 50
Name: BIOL 3003 Exam 1 Study Guide
Description: This study guide covers chapters 1, 2, 3, 8, and 9 which will be on the first lecture exam. They include all important mechanisms, terms, and concepts, as well as a quick background on the discovery of DNA and other things that we should know. I condensed lecture video information as well as key topics from the textbook into a quick, easy to read outline to guide your studying.
Uploaded: 06/01/2019
10 Pages 4 Views 9 Unlocks
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Hannah Pope (Rating: )



Summer 2019 Dr. Wooten


what is Eukaryotic Replication?



BIOL 3003 EXAM 1

1. MAIN TOPICS

A. History of Discovery

i. genetics/ heredity, DNA structure and replication, condensation B. Cell Replication

i. Prokaryotic Replication: 1 large circular plasmid DNA, one origin ii. Eukaryotic Replication: many large linear chromosomes, multiple origin sites, linear DNA tightly packed around histone proteins

2. GENETICS OVERVIEW

A. Genetics: branch of biology dealing with heredity (transmission of  traits across generations, genotype vs phenotype) and expression of  inherited traits (detectable phenotype variation of character) through  genetic material  phenotypic character, genetic processing/  regulation, mutation, and proofreading Don't forget about the age old question of What is common ion effect?

1. Molecular: chemical nature of gene (structure, organization, function of DNA/ encoding, replicating, expressing)  

2. Transmission: classical heredity, how traits of individuals pass on


what is genetics?



3. Population: how traits of group change over time  

(evolution)

4. Etymological:  

ii. genotype: inherited DNA, set of alleles (Aa, AA, or aa)

1. homozygous: same alleles (aa or AA) | heterozygous:  

different alleles (Aa)

iii. phenotype: variant embodiment of character

iv. gene: inherited factor for characteristic

v. allele: inherited versions of genes, represent DNA sequences (A=  normal) We also discuss several other topics like what is Advertising?

vi. locus: location of allele (gene) on chromosome

vii. characteristic: attribute of organism  

viii. epigenetics: Affecting your DNA (genome) by lifestyle  (environmental input, such as nutrition) which is passed on (as the  epigenome)

1. model genetic organism: for genetic analysis

3. HISTORY OF GENETICS

i. Human observation  Theories  Science + History (shape societal  ideas)

ii. Domestication 1000 yrs ago: root of genetics


what is genotype?



1. Observation  breeding  modification of species

2. Began in Fertile Crescent of Mesopotamia (middle east),  movement was West to East because north had mountains,  south had desert

3. Began huningt/ gathering plants (cereal grain/ granames,  silos, date palms), breed animals (goats, sheep, gazelles,  dogs, horses)  settled communities to start science (with  irrigation and permanent buildings)  

 iii. Spontaneous Generation: (10,000 years ago- 1850)  1. “Things just occur, 1 form to another, w/o descent from  similar species” We also discuss several other topics like What are the difference in the North Atlantic Slave Trade and African slavery?
We also discuss several other topics like Why can’t self­ determination go very far in world politics?

2. Evidence: alchemy, seeing a carcass turn into worms/ flies a. Religion: praying to deities (Venus of Willendorf for  If you want to learn more check out What is The knights of labor?

pregnancy 22,000 years ago) and Christianity (“let waters bring forth living creatures)

b. Aristotle: “grow spontaneously, not from kindred”

c. Shakespeare: “serpent and crocodile bred from your  mud’’

3. Disproven: by Pasteur (1859) showed closed flasks grew no  life over time

iv. Preformationism (1600’s):  

1. “Organisms develop from mini versions of themselves” a. suggests that all organisms were created at the same time,  and that succeeding generations grow from homunculi,  

or animalcules, that have existed since the beginning of  

creation 

2. Influence: Enlightenment, Greek writings, early microscopes a. William Harvey (1651): ovist preformationist theory that  all organisms come from eggs “ex ovo omnia” fertilization occurred through a mysterious transference by contact  b. Antoine van Levenhock: sperm is vessel for tiny person  (after discovering spermatozoa) We also discuss several other topics like What is plasmids?

i. Homunculus diagram by Nicolass Hartsoeker, 1694 2

c. Alfigen: egg is vessel for tiny person

3. Disproven: microscopes and early technology

v. Pangenesis (1800’s)

1. “Body cells shed Gemules (small pieces of selves) throughout life, which collect in reproductive organs before fertilization” 2. Influence: Blended Inheritance (avg) and Acquired  Characteristics (you gain stuff and pass it on, a theory that Darwin contributed to but ultimately disproved, claimed it  was an “unverified hypothesis”)

a. Lamarckism: pass on learned skills (similar to acquired  characteristics); If an organism changes to adapt to its  

environment in its lifetime, those changes are passed on  to offspring  

i. Ex: giraffe necks growing to reach trees, passing  that on

b. Darwinism: organisms, even of the same species, are all  different; those with good variations survive and mate  

3. Disproven: by Weissman

a. white rabbits with black ovaries made black babies (no  inheritance)  

b. Rat tail mutation: chopping off tails and breeding 32  generations, babies still had long tails

vi. Epigenesis: now generally held theory that an embryo develops  progressively from an undifferentiated egg cell (every part arises  new through development)  

1. Only thing passed on is instructions, nothing physical 2. “De Novo/ Germ Plasm Theory”, embryo not preformed but  grows

vii. Epigenetics: (some similarities to Lamarckism) after 8 weeks,  environmental factors determine genetic activity (genes on or off)  that is inheritable

4. MOLECULAR GENETICS: GENETIC INFORMATION  (STRUCTURE AND GENOTYPE)  

i. Successful genetic material…

1. Stores complex information, capable of encoding phenotype 2. Replicate faithfully, can mutate

ii. History of Discovery

1. The Basics

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a. 1869, 1871: Freidrich Mieschner isolated nuclein (DNA)  from used bandages/ salmon sperm

b. 1885, 1901: Albert Kossel isolated and identified genetic material “nucleic acid” in nucleus, didn’t know function c. 1878: Warther Flemming found nucleic acid makes up  chromatin in nucleus, and proteins involved in heredity  d. (Chemical structure) Phoebus Levebe: RNA 1901, DNA  1929

2. Transforming Principles

a. 1927: Griffith, studying pneumonia & “can dead bacteria  genetically transform living cells?”, discovered  

bacterial transformation  

i. (mice injected with non-virulent and heat killed  virulent die, so heat killed virulent transforms non virulent)

b. 1944: Avery, McLeod, McCarty Q “what was the  transforming agent”

i. Heat killed cells treated with RNase, protease, and  DNase, all transformed except for those with  

DNase, with no DNA which was responsible for the  chemistry of transformation

ii. Chromatin = DNA (transforming principle) +  

proteins

3. DNA is the biomolecule of heredity

a. 1952: Hershey + Chase, bacteriophage prove DNA is  genetic material  

1. Integrated DNA with P-32, protein with S (radioactive) in a phage, which is a virus with naked DNA (no  

chromatin)  

2. Replicated (phage takes over bacteria and uses its  

genetic process to replicate)  only P-32 passed  

through and made R phages, so DNA, not protein, is

the genetic material

4. Chemical components, physical structure & molecular form  of DNA

a. 1944- 1952: Erwin Chargaff disprove nucleotide  

hypothesis A=T=C=G

i. Described ratios using DNA in viruses fungi, E coli  (equal) flies, humans (different)  A=T, C=G  A+G  =C+T in dsDNA

ii. High G=C correlates with thermostability (primitive) 4

iii. Linus Pauling: hypothesized triple helix, disproved  bc:

1. – phosphates near axis and too short Van der Waal  

distances  

b. 1953: Watson + Crick (Cambridge)

i. Proposed base pairing was parallel, discovered  double helix DNA structure and anti-parallel  

base pairing

ii. Rosalind Franklin (King’s College)

1. X-ray diffraction to obtain pieces of DNA molecule 

physical evidence it’s a 3 part model (later will be  

known to be 1. nucleotide, 2. phosphate, and 3. sugar)

5. Chemical structure of DNA

i. Phoebus Levene: RNA 1901, DNA 1929

ii. 1957 Alexander Todd: synthesis of nucleotides b. DNA: Deoxyribonucleic Acid, chemical unit of inheritable  info made of

i. Nitrogenous Base (Nucleotide)

1. 6 membered Pyrimidine: Cytosine, or Thymine (Uracil in DNA)

2. 9- membered Purine: Adenine or Guanine

ii. Sugar: Deoxyribose sugar (DNA) or Ribose sugar  (RNA)

1. C1: base attachment (A,T, G, C, U)

2. C2: DNA (H) vs RNA (OH)

3. C3: 3’5’ LINKAGE

4. C5: phosphodiester bond

iii. Phosphoric Acid (PO4): links nucleotides

c. Watson + Crick models of DNA

1. 2 right handed polynucleotide chains coil around  

central axis (anti-parallel, complementary) 2 nm wide  

helix

2. Bases are flat, perpendicular to central axis, stacked  0.34 nm (# bases)^4 = # possible combinations

ii. A form DNA: condensed, 2.3 nm wide, 11 base  pairs/ turn

iii. B form DNA (Watson + Crick Model): common, 3.4 nm wide, 10 base pairs/ turn, pH 7 (aqueous in  low salt)

5

iv. Z form DNA: left-handed, reversed, comes from A  form, 12 base pairs/ turn, in transcriptional areas

5. DNA REPLICATION/ SYNTHESIS (S PHASE)

A. Ensures each cell in organism has a complete/ correct copy of the  genome to live  

i. Fast: 5 million bp/ chromosome/ hour for E coli, 6 million bp/ cell/  few hours

ii. High fidelity: only 1 error every billion nucleotides due to proof reading and error checking mechanisms

iii. G1: loose strand  homolog to replicate – S phase  sister  chromatids post-replication, join by kinetochore/ centromere B. History of Discovery

i. 1957: discovery of semi conservative replication by Taylor,  Woods, Hughes

1. 3 possible types of DNA replication:  

a. conservative (parental+parental and new+new)  

b. dispersive (par/new + par/new and par/new+par/new  caused by each parental strand cleaving and reforming  with new)

c. semi-conservative (parental+new and parental+new)  i. proven by Taylor, Woods, and Hughes: radiated  fava bean root tips, replicate, saw 1 radiant  

“parental” chromatid

ii. 1959: Arthur Kornberg discovers DNA Polymerase and synthesis mechanism

C. 4 Major Steps

a. Semi-conservative, bidirectional (both parental strands  replicated at once, lagging/ leading)  

2. INITIATION

a. Initiator protein binds to one of 30,000- 50,000 origin  (OriC) points in strand (rich in A and T)

b. Replication bubbles grow bidirectionally due to DnaA  protein box (replication initiation factor which promotes  the unwinding of DNA) 

i. Positive control of replication: “licensing”  

1. each origin must be bound by  

a. ORC (Origin Recognition Complex) throughout DNA

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b. Licensing factors: accessory proteins cdt-6 and  

cdt-1 go to ORC, coat DNA q/ MCM proteins for  

replication, leave after S phase and MCM proteins  

go to front of replication fork, reattach after mitosis

ii. Negative control of replication (after S phase, at  G2): Gemini protein blocks cdt-1 and thus prevents assembly of MCM proteins on new DNA  

a. Degraded during mitosis so daughter cells can  

respond to positive control of replication

(licensing factors) & replicate

3. UNWINDING

a. Topoisomerase (gyrase): reduces torsional strain b. Helicase breaks hydrogen bonds between  

complementary nucleotides

c. ss binding proteins stabilize/ hold open ssDNA

4. PRIMER SYNTHESIS

a. Primase (a type of RNA Polymerase) adds a nucleotide  primer to ssDNA (5-10 nucleotides long)  

b. DNA polymerase III attaches to 3’ end of RNA primer 5. ELONGATION

a. DNA Polymerases  DNA Pol III elongates, DNA Pol II, IV,  and V repair DNA, DNA Pol I removes RNA primer on 3’ OH b. New DNA strand synthesized from dNTPs (dATP, dGTP,  etc),  

c. 3’ OH of last nucleotide on strand attacks 5’ PO4 of  incoming dNTP

d. A phosphodiester bond forms between 2 nucleotides ii. Proofreading by DNA Pol II, IV, V: mistakes are rare,  1:100,000,000 bases

1. Triggered by instability of mismatched base pairs

2. Configuration of DNA Pol I active site proofreads and  exonucleates (knocks off and replaces base)

iii. Trombone model of replication: DNA Pol III simultaneously grabs  leading and lagging strands in the same direction  

1. Leading strand: naturally synthesized 3’  5’

2. Lagging strand: many short sequences (Okazaki  fragments) started off with many primers to synthesize 3’5’, joined by DNA Ligase by making covalent phosphodiester  bonds

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iv. Telomeres: repeat DNA and protein complex at ends to seal/  protect DNA

a. Telomerase: riboprotinate enzyme (RNA) binds to DNA at unreplicated overhang caps, slightly shorter new strand  because primers removed, also aged by obesity

6. DNA CONDENSATION

i. 46 chromosomes in somatic human cell = 6 million base pairs = 2  meters of DNA

1. Large DNA molecules must be condensed to fit within cell  nucleus

B. History of DNA Models- Protein Association

i. 1965, Folded Fiber Model: EJ Dupraw found few free fiber ends  “each chromatid has 1 fiber”

ii. 1974, Nucleosome: simplest packaging structure of chromatin,  reduces length by 7x, each coils 200 base pairs held together by  electrostatic bonding, because the histone is positive and DNA is  negative

C. Cell Division Overview, by length

i. G1 phase: Making chromatin

1. 2 nm coiled dsDNA  wraps into nucleosomes (or  

chromatosome if at end with histone tail) which contains an  8 histone core (2x of H2A, H2B, H3, H4, 120 amino acids  each, highly conserved), and H1 histone (loosely associated  with core particle, has many functions besides holding  

nucleosome in place, not conserved, changes between tissue types)

ii. S phase: Supercoiling chromatosomes

1. H1 histone induces DNA compacting, pulls together 5 or 6  nucleosomes into a zig zag (center filled with DNA) or  

solenoid (donut shape)

2. Chromatin hub opens DNA to read in zig zag protein for  transcription

3. Linker DNA is straight (connects opposite nucleosomes) so  supercoiled solenoids aren’t flexible

iii. G2 phase: Higher order coiling, supercoiling of supercoil =  chromatin

1. Make 300 nm “chromatin loops”, scaffold around non-histone proteins= rosettes of chromatin loops

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2. These stack 250 nm wide, 700 nm tall into a chromatid in  the final shortening/ thickening around protein scaffold  (mechanism unknown, “blackbox”)  

7. MENDELEIAN GENETICS

A. Heredity principles: how genes are passed from generation to  generation and how factors influence inheritance

i. Gene: inherited factor for characteristic  

ii. Allele: inherited versions of genes, represent DNA sequences (A=  normal)

iii. Locus: location of allele/ gene on chromosome

iv. Genotype: set of alleles, AA, aa (homozygous) or Aa (heterozygous) v. Phenotype: trait (physical manifestation of trait)

vi. Characteristic: attribute of organism

vii. reciprocal cross: white x black

viii. backcross: F1 and either parental cross

B. Gregor Mendel (1822- 1884): ordained priest and teacher,  experimented on Psium Satium 1856-1863, presented 1865, success  due to pea plants’ quick reproduction (1 year), starkly different  characteristic focus, used math and observed theories

i. Main Q: “is blending inheritance the cause of heredity?” ii. Monohybrid Cross: bred homozygous pure-breeding plants  differing in 1 trait

a. P gen: AA x aa

b. Flial 1 (F1) gen: all Aa

c. F2 gen: 3 A_, 1 aa

2. 1st mode of inheritance: Concept of Dominance  when  2 different alleles are present in a genotype (Aa), only  

dominant allele (A) shows

3. Simple mendeleian conclusions

a. 1st Law: Principle of Segregation, meiosis random  separation of homologs into gametes, each organism has  2 alleles (1 from each parent) which separate equally  

during gamete formation

b. 2nd Law: Principle of Independent Assortment,  Alleles at different loci separate independently and  

equally (if on same chromosome, they don’t assort)  

during meiosis anaphase II (2x meiosis cycles)

iii. Dihybrid cross: differ in 2 charecteristics

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1. P gen: PPYY x ppyy

2. F1 gen: all PpYy with PY, py, pY, Py gametes

3. F2 gen: 9 P_Y_ : 3 P_yy : 3 ppY_ : ppyy

C. Probability

i. 1st: Multiplicatio Rule “AND”  Prob. of 2 independent events =  P1 x P2

ii. 2nd: Addition Rule “OR”  prob. of 2 mutually exclusive events  = P1 + P2

iii. Test cross: T_ x tt (if TT: all T_, if Tt: 3 T_: 1 tt)

D. Mendel’s 6 Big Crosses

 

 

RY

Ry

rY

ry

RY

RR

Y

Y

RR

Y

y

RrY

Y

RrY

y

Ry

RR

Y

y

RR

y

y

RrY

y

Rry

y

rY

RrY

y

RrY

y

rrY

Y

rrY

y

ry

RrY

y

Rry

y

rrY

y

rry

y

10

Final assortment ratio  (phenotypic): found by  multiplying monohybrid  segregation ratios (also  phenotypic)  

Rr x Rr  3:1

RrYy x rryy  1:1:1:1

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