Genetics Flashcards

1
Q

Elements of Nucleic Acids

A

CHONP

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2
Q

Elements of Proteins

A

CHONS

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3
Q

Purines

A

Double ringed nitrogenous bases
Guanine and Adenine

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4
Q

Pyrimidines

A

Single-ringed nitrogenous bases
Cytosine, Thymine, Uracil

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5
Q

DNA vs RNA

A

RNA contains ribose instead of deoxyribose and RNA is the primer for DNA replication. Also used for Gene Expression

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6
Q

Significance of 5’ and 3’ ends on Nucleotides

A

Nucleotides have 5 carbons. Nitrogenous bases attach at 1’ carbon, phosphate groups are attached to the 5’ carbon. Nucleotides connect with each other at the 5’ and 3’ ends.

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7
Q

What causes the double-helix shape of DNA?

A

Strong hydrogen bonds cause each strand to curl around each other, creating double-helix shape

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8
Q

How are DNA strands read? How are they built?

A

Read: 3’ –> 5’
Built: 5’ –> 3’
Why? DNA strands are anti-parallel.

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9
Q

Griffith

A

Discovered that bacteria can transfer genetic information through a biochemical agent (tested rats with pneumonia because of the capsule of the pathogenic var. and the non-capsule var.)

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10
Q

Avery, Macleod & McCarty

A

discovered that DNA was the genetic factor that caused the death of Griffith’s mice, not protein. used enzymes (DNAse & Proteases) to prove it

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11
Q

Chargaff

A

determined the ratios of the four DNA nucleotides. His work provided evidence of the base pairing rules. (grinded up animal meat and noticed different percentages of certain nucleotides, like 20% G 20% C 30% A 30% T)

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12
Q

Hershey & Chase

A

Proved genetic information was made from DNA (not protein) by seeing which radio-labeled molecule was injected into infected bacteria by viruses

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13
Q

Franklin

A

used x-ray diffraction to detect the shape of DNA

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14
Q

Crick & Watson

A

did not do any experiments, made models using data from previous experiments (Franklin) and described the double-helix structure of DNA (suggested DNA could act as a template for making more DNA and could mutate)

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15
Q

Enzymes of DNA Replication in order

A
  1. Helicase
  2. Primase
  3. DNA Polymerase III
  4. DNA Polymerase I
  5. Ligase
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16
Q

DNA Replication

Helicase

A

opens up DNA at the origin and creates replication fork

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17
Q

DNA Replication

Primase

A

builds RNA primer piece in the 5’ –> 3’ direction

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18
Q

DNA Replication

DNA Polymerase III

A

builds the DNA strands by adding nucleotides to the RNA primer and immediately checks and replaces incorrect bases

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19
Q

Leading Strand

A

continuously synthesized strand of DNA in the 5’ –> 3’ direction

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20
Q

Lagging Strand

A

discontinuously synthesized strand that creates short segments called Okazaki fragments

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21
Q

DNA Replication

DNA Polymerase I

A

replaces RNA primers with DNA

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22
Q

DNA Replication

Ligase

A

joins all the Okazaki fragments together

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23
Q

Semi-Conservative

A

After replication, each chromosome retains an old copy of the DNA and a new copy that was newly synthesized

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24
Q

Mutation Repair

DNA Polymerase III

A

corrects DNA base errors replication itself

25
# Mutation Repair DNA Polymerase I
immediately corrects DNA base errors AFTER replication
26
# Mutation Repair Excision Repair
DNAses cut out damaged DNA DNA Polymerases synthesize DNA DNA Ligases piece DNA back together
27
# Mutation Repair Photoactivation
Photolysases are light activated and repair DNA IN BACTERIA ONLY
28
Xeroderma Pigmentosum
patients lack DNA repair system in skin cells causing higher rates of mutation (thymine dimers). No protection from UV and results in multiple skin cancers prior to age 20.
29
Gene Expression Steps
1. Transcription 2. Translation
30
Transcription
**Initiation**: RNA Polymerase binds to promoter region (TATA box) and unzips DNA **Elongation**: RNA Polymerase makes one RNA strand from one DNA template using RNA nucleotide **Termination**: RNA Polymerase reaches termination site and transcript is released
31
Translation
**Initiation**: mRNA binds to small ribosome subunit. 1st tRNA ANTIcodon binds to mRNA START codon bringing MET to the P-site. Large ribosome subunit binds so translation machinery is set up and ready for use **Elongation**: 2nd tRNA binds to 2nd mRNA codon at A-site bringing 2nd amino acid. 1st and 2nd aa form peptide bond and produces dipeptide. Ribosome translocates along mRNA by one codon so dipeptide at P-site, new codon is at A-site and old empty tRNA departs from E-site. 3rd RNA codon at A-site **Termination**: Ribsome reaches stop codon (UAG, UGA, UAA) at A-site and translation stops. Polypeptide is released and ribosome subunits disband.
32
Constitutive Genes
permanently expressed genes since their products are essential (ATP)
33
Operons
groups of structural genes that can be turned off or on in response to environmental conditions
34
Repressible operon
genes that are typically expressed. turned off when end product is no longer needed. Anabolic
35
Inducible operon
genes typically silent/not expressed. Turned on when inducer (substrate or enzyme pathway) enters cell. Catabolic
36
Lactose Operon
1. Repressor protein (I Gene product) is attached to operator site and blocks operon expression 2. RNA polymerase at promoter site is blocked and can't transcribe structural genes 3. Lactose INDUCES operon ON and inactivates Repressor protein so operator is not blocked anymore 4. RNA Polymerase binds to promoter and transcribes mRNAs which are translated into enzyme proteins - OPERON STRUCTURAL GENES are not expressed and enzyme products catabolize LACTOSE needed
37
# Protein Folding 1° structure
straight amino acid structure sequence
38
# Protein Folding 2° structure
pleating/helical structure formed from intermolecular bonds (helix-shaped)
39
# Protein Folding 3° structure
3D protein folding upon itself
40
# Protein Folding 4° strucure
two or more polypeptides interfolded together
41
# Protein Folding Prion Diseases
Prions are misfolded proteins. These misfolded proteins cause others to change and disrupts the normal functioning
42
Spontaneous Mutation
Mistakes just happen and are not always corrected (during replication or at any time)
43
Mutagens
substances that increase the number of mutations above the spontaneous rate
44
Types of Mutagens
* Chemical: benzene, aflatoxin, cigarette smoke, base analogs * Physical: Ionizing (x-rays, gamma rays) and Non-Ionizing (UV creating Thymine Dimers) * Biological: HPV (cervical cancer), Hep B (liver cancer)
45
# Point Mutations on Gene Expression Same Sense
Same/similar amino acid incorporated. Product = same polypeptide | Thh cat sat onn the mat. ## Footnote Substitution Mutation
46
# Point Mutations on Gene Expression Missense
Different amino acid inserted into polypeptide. Products = non-functioning protein/structure | The bat sat onn the mat. ## Footnote Substitution Mutation
47
# Point Mutations on Gene Expression Nonsense
Stop codon sequence inserted into polypeptide --> terminated. Product = short peptide | The cat. ## Footnote Substitution Mutation
48
# Point Mutations on Gene Expression Frameshift
every codon is misread if nucleotides are not added/lost in triplets. Product = VERY different protein | The eca tsa ton nth ema t. ## Footnote Addition/Deletion Mutation
49
# Transfer of Beneficial Mutations Transformation
Uptake of DEAD cell DNA by DNA TRANSPORTER protein into living recipient --> **recombinant**
50
# Transfer of Beneficial Mutations Conjugation
F+ donor has F PLASMID and produces sex pili to attach to recipeint cell. Rolling copy of plasmid DNA passes from donor to F- recipient along conjugation bridge --> **Recombinant F+ cell**
51
# Transfer of Beneficial Mutations Hfr (high frequency) conjugation
Hfr+ donor cell sends rolling copy of both plasmid genes and adjacent chromosomal genes to F- recipient --> **Recombinant Hfr+ cell**
52
# Transfer of Beneficial Mutations Transduction
bacteriophage picks up bacterial genes and transfers them from 1st bacterial host to 2nd --> **Recombinant cell **
53
# Transfer of Beneficial Mutations Transposons
jumping genes jump around chromosome and between bacterial cells --> **Recombinant cells**
54
Results of bacterial mutations?
* bacterial populations develop increased virulence, increased ABX resitistance, and increased disinfectant resistance * Beneficial mutants multipily and spread if there's "selection pressure" * Over time, we would face the inability to treat infections, increase in patient suffering and mortality ## Footnote overuse of ABX creates selection pressure for ABX resistant pathogen survivors
55
Ames Test
test used to test the potenital mutagenic factors of some chemicals using "wild" Salmonella
56
# Ames Test Auxotroph Mutant
His- mutant that could not grow on minimal medium
57
# Ames Test Back-Mutant/Revertant
Mutant "mutant" that mutates back to normal (spontaneous mutation) (His- --> His+)
58
# Ames Test Potential Mutagen
His- mutants are exposed to a factor and can mutate back to normal His+. The more colonies that grow, the more suspicious the factor is mutagenic