1A: information molecule that is passed on is DNA: how do we know this? Flashcards

1
Q

what is genetics?

A

study of heredity and variation in cells, individuals, and populations

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2
Q

what are 2 definitions of genes?

A

1) a functional unit of heredity and variation

2) DNA sequence involved in making RNA and protein

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3
Q

what is molecular genetics?

A

the study of structure and function of genes at the molecular level

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4
Q

what are alleles?

A

variant form of a gene cause by difference in DNA sequence

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5
Q

what is a genotype?

A

gene/genes inherited by organism

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6
Q

what is a phenotype?

A

visible traits (ex: body plan, behaviour, illnesses/diseases)

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7
Q

what is a genome?

A

the entire DNA sequence of an organism

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8
Q

what is gene expression?

A

“turning on” a gene to produce RNA/protein

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9
Q

what are 2 types of RNA that genes can produce?

A

1) coding RNA

2) noncoding RNA

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10
Q

what does it mean if RNA is coding and what kind of RNA is coding?

A

it means those pieces of RNA produce protein

mRNA

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11
Q

what does it mean if RNA is noncoding and what kind of RNA is noncoding?

A

it means they do not produce proteins, have other functions.

tRNA, rRNA

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12
Q

what happens when a gene is “turned on”?

A

the code from that gene is transcripted to RNA, which then may or may not translate and produce protein (the RNA may serve some other function though)

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13
Q

what is protein expression?

A

the type and abundance of proteins in the cell

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14
Q

what component ultimately determines the phenotype of the cell? explain

A

proteins. DNA directly protein expression, but proteins ultimately control phenotype because they control every reaction in the cell

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15
Q

what do enzymes do?

A

catalyze the synthesis and transformation of all biomolecules

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16
Q

what do structural proteins do?

A

maintain cell shape

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17
Q

what are signalling proteins?

A

hormones and receptors

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18
Q

what 2 things cause phenotypic variation?

A

1) difference in alleles (slight variation in gene sequence results in changes in amino acid sequence of proteins)
2) differential regulation of gene and protein expression

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19
Q

what is the purpose of sequencing genomes?

A

to understand how the types and abundance of RNA and proteins result in the phenotype of an organism

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20
Q

what are 5 fields that benefit from the study of molecular genetics?

A
  • human health
  • forensic
  • agriculture
  • environment
  • evolutionary biology
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21
Q

how does studying molecular genetics affect the field of human health?

A

better understanding of human diseases/conditions results in new therapeutics and diagnostics

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22
Q

how does studying molecular genetics affect the field of forensics?

A

allows DNA fingerprinting, which can be used to solve crimes, do paternity tests, match organ donors, authenticate consumables, and find the source of food poisoning outbreaks

23
Q

how does studying molecular genetics affect the field of agriculture?

A

superior crops and livestock (“pharm” animals) can be bred/engineered

24
Q

how does studying molecular genetics affect the field of environment?

A

molecular ecology allows species identification and diagnosis for conservation and species-habitat relationships.
allows microbes to be genetically engineered for bioremediation (treatment of contaminated stuff)

25
Q

how does studying molecular genetics affect the field of evolutionary biology?

A

development of phylogenetics (study of evolutionary history and relationships among or within groups of organisms) and phylogenomics (intersection between fields of evolution and genomics)

26
Q

why is the S strain of Streptococcus pneumoniae virulent but the R strain isn’t?

A

the S (smooth) strain is surrounded by a polysaccharide capsule (which creates a smooth, kind of slimy sugar coating) that protects it from the immune system. the R (rough) strain does not have this and is therefore wiped out by the immune system before it can do a lot of damage to the host.

27
Q

what was Griffith’s experiment? what were his findings?

A

injected S strain and R strain Streptococcus pneumoniae cells into mice.

his findings: when mice are injected with…

1) live S strain, they die.
2) live R strain, mice live, no live R cells are found in their blood.
3) heat-killed S cells, they live, no live S cells in their blood.
4) heat-killed S cells and living R cells, they die, live S cells found in blood

28
Q

what did Griffith conclude from his experiment?

A

R cells exposed to dead S cells transformed permanently into S cells, and passed this down to their offspring. this is done through some molecule (the transforming principle) released when S cells are killed that change the R cells.

29
Q

what is the transforming principle?

A

the molecule released from cells when they are killed, which causes transformation in other cells into the cells that died. (the agent responsible for transformation)

30
Q

what is transformation?

A

permanent, heritable change when a cell is converted into another cell after being exposed to its transforming principle molecule.

31
Q

what were the potential things the transforming principle was thought to potentially be? which one was favoured by the scientific community at the time and why?

A

DNA, RNA, or proteins.
proteins were thought to be most likely because of the large variety of amino acids that comprise them. DNA and RNA were thought to not be complex enough to be the material of genetics.

32
Q

what was the logic behind Avery, MacLeod, and McCarthy’s experiment? what was the experiment, outcome, and conclusion?

A

eliminating each of the potential transforming principle molecules and see whether the transformation of R cells to S cells still occurs. if transformation does not occur, then the eliminated substance must have been the transforming principle.

the steps:

1) mix RNAse into cell extract of heat-killed S cells (so DNA and proteins are left over)
outcome: transformed
2) mix protease into cell extract of heat-killed S cells (so RNA and DNA are left over)
outcome: transformed
3) mix DNAse into cell extract of heat-killed S cells (so RNA and proteins are left over)
outcome: no transformation
conclusion: DNA must be the transforming principle

33
Q

what is the general structure of a virus?

A

one or more nucleic acid molecules surrounded by a protein coat

34
Q

what is a capsid?

A

the protein coat surrounding a virus

35
Q

what is an envelope?

A

a membrane that surrounds the capsid, derived from the host cell’s cell membrane (not all viruses have one)

36
Q

what genes do all viruses have?

A

the genes that encode their coat proteins and that encode proteins involved in the regulation of transcription

37
Q

what gene must all enveloped viruses have?

A

genes requires for synthesis of envelope proteins

38
Q

what are the two basic structures of viruses?

A
  • helical

- polyhedral

39
Q

what is the difference between helical and polyhedral viruses?

A

helical: protein subunits assemble in a rod-like spiral around the genome
polyhedral: coat proteins form triangular units that fit together like patches on a soccer ball. some have recognition proteins that extend like spikes from the corners.

40
Q

what is a bacteriophage/phage?

A

a virus that affects bacteria

41
Q

what are virions?

A

the progeny viruses produced inside the host cell

42
Q

what is a virulent bacteriophage?

A

viruses that kill their hosts during each cycle of infection

43
Q

what is a temperate bacteriophage?

A

viruses that enter an inactive phase while inside the host cell and can be passed on to several generations of daughter cells before becoming active and killing their host

44
Q

what virulent bacteriophages have been most valuable in genetic studies?

A

T-even bacteriophages (T2, T4, T6)

45
Q

what is the structure of T-even bacteriophages?

A
  • body separated into head and tail
  • double-stranded linear molecule of DNA is packed into head
  • tail is made of proteins and has recognition proteins on its tip that can bind to the surface of a host cell
46
Q

describe the infective cycle of a T-even bacteriophage

A

1) phage attached to host cell by tail. enzyme in viral coat digests hole in the cell wall
2) phage injects its DNA into cell. rest of the protein (capsid) remains outside. phage uses host machinery to produce different proteins.
3) eventually 100-200 viral DNA molecules are synthesized
4) viral heads and tails are synthesized
5) head and tail are assembled and viral DNA is packed into the heads (virions are formed)
6) lysozome lyses bacterial cell wall, causing it to rupture and release all the virions

47
Q

what is the infective cycle of T-even bacteria called?

A

the lytic cycle

48
Q

what are the steps of the lysogenic cycle?

A

1) phage injects its DNA into bacterium
2) viral DNA forms a circle (at this point the cell may enter the lytic cycle)
3) viral DNA integrates into a specific site of the bacterial DNA by crossing over. gene on prophage is expressed to produce a repressor protein that blocks expression of lytic cycle genes
4) prophage is replicated with rest of bacterial DNA when the cell divides
5) each daughter cell has a prophage
6) eventually (usually due to some stressful event) repressor protein is deactivated and destroyed–the prophage exits the bacterial DNA and the virus enters the lytic cycle

49
Q

what is a prophage?

A

viral DNA while it is insterted in the host cell DNA

50
Q

what can trigger transition from the lysogenic to lytic cycle?

A

environmental signals such as nutrient availability or UV radiation, or stress

51
Q

what is specialized transduction?

A

transfer through viruses of genes from one cell to another. when exiting the lysogenic cycle, some of the host DNA may be removed with the prophage, and this can make its way into other cells.

52
Q

what is the difference between bacteriophages and animal viruses?

A

animal viruses may enter the cell entirely, with their protein coat still attached. (though the envelope never enters)

53
Q

what is a latent phase?

A

like the lysogenic phase but in animal viruses