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microbio > Genetics > Flashcards

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
Q

Mutation Repair

DNA Polymerase I

A

immediately corrects DNA base errors AFTER replication

26
Q

Mutation Repair

Excision Repair

A

DNAses cut out damaged DNA
DNA Polymerases synthesize DNA
DNA Ligases piece DNA back together

27
Q

Mutation Repair

Photoactivation

A

Photolysases are light activated and repair DNA
IN BACTERIA ONLY

28
Q

Xeroderma Pigmentosum

A

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
Q

Gene Expression Steps

A
  1. Transcription
  2. Translation
30
Q

Transcription

A

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
Q

Translation

A

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
Q

Constitutive Genes

A

permanently expressed genes since their products are essential (ATP)

33
Q

Operons

A

groups of structural genes that can be turned off or on in response to environmental conditions

34
Q

Repressible operon

A

genes that are typically expressed. turned off when end product is no longer needed. Anabolic

35
Q

Inducible operon

A

genes typically silent/not expressed. Turned on when inducer (substrate or enzyme pathway) enters cell. Catabolic

36
Q

Lactose Operon

A
  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
Q

Protein Folding

1° structure

A

straight amino acid structure sequence

38
Q

Protein Folding

2° structure

A

pleating/helical structure formed from intermolecular bonds (helix-shaped)

39
Q

Protein Folding

3° structure

A

3D protein folding upon itself

40
Q

Protein Folding

4° strucure

A

two or more polypeptides interfolded together

41
Q

Protein Folding

Prion Diseases

A

Prions are misfolded proteins. These misfolded proteins cause others to change and disrupts the normal functioning

42
Q

Spontaneous Mutation

A

Mistakes just happen and are not always corrected (during replication or at any time)

43
Q

Mutagens

A

substances that increase the number of mutations above the spontaneous rate

44
Q

Types of Mutagens

A
  • 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
Q

Point Mutations on Gene Expression

Same Sense

A

Same/similar amino acid incorporated. Product = same polypeptide

Thh cat sat onn the mat.

Substitution Mutation

46
Q

Point Mutations on Gene Expression

Missense

A

Different amino acid inserted into polypeptide. Products = non-functioning protein/structure

The bat sat onn the mat.

Substitution Mutation

47
Q

Point Mutations on Gene Expression

Nonsense

A

Stop codon sequence inserted into polypeptide –> terminated. Product = short peptide

The cat.

Substitution Mutation

48
Q

Point Mutations on Gene Expression

Frameshift

A

every codon is misread if nucleotides are not added/lost in triplets. Product = VERY different protein

The eca tsa ton nth ema t.

Addition/Deletion Mutation

49
Q

Transfer of Beneficial Mutations

Transformation

A

Uptake of DEAD cell DNA by DNA TRANSPORTER protein into living recipient –> recombinant

50
Q

Transfer of Beneficial Mutations

Conjugation

A

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
Q

Transfer of Beneficial Mutations

Hfr (high frequency) conjugation

A

Hfr+ donor cell sends rolling copy of both plasmid genes and adjacent chromosomal genes to F- recipient –> Recombinant Hfr+ cell

52
Q

Transfer of Beneficial Mutations

Transduction

A

bacteriophage picks up bacterial genes and transfers them from 1st bacterial host to 2nd –> **Recombinant cell **

53
Q

Transfer of Beneficial Mutations

Transposons

A

jumping genes jump around chromosome and between bacterial cells –> Recombinant cells

54
Q

Results of bacterial mutations?

A
  • 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

overuse of ABX creates selection pressure for ABX resistant pathogen survivors

55
Q

Ames Test

A

test used to test the potenital mutagenic factors of some chemicals using “wild” Salmonella

56
Q

Ames Test

Auxotroph Mutant

A

His- mutant that could not grow on minimal medium

57
Q

Ames Test

Back-Mutant/Revertant

A

Mutant “mutant” that mutates back to normal (spontaneous mutation) (His- –> His+)

58
Q

Ames Test

Potential Mutagen

A

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

microbio (17 decks)

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