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Fall 2022 > Biology Midterm - Cycle 1-6 > Flashcards

Biology Midterm - Cycle 1-6 Flashcards

1
Q

What is the difference between eukaryotes and prokaryotes?

A

Eukaryotes: linear DNA and membrane bound nucleus
Prokaryotes: circular DNA and no nucleus

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2
Q

How do prokaryotes and eukaryotes reproduce?

A

binary fission vs mitosis/meiosis

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3
Q

Examples of eukaryotes?

A

Multicellular: animals (metazoans), plants, some fungi
Unicellular: protists, some fungi

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4
Q

examples of prokaryotes?

A

Bacteria and Archaea

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5
Q

Why are viruses not cellular life?

A
  • not made of cells so they cannot create proteins on their own
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6
Q

What are obligate parasites?

A

VIRUSES - must infect a host cell to create proteins and replicate

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7
Q

What is the structure of a virus?

A

protein shell (some with lipid envelope) with NUCLEIC ACID genome - DNA or RNA; single or double stranded

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8
Q

What is HIV?

A
  • type of simian IV - retrovirus
  • causes AIDS
  • disrupts immune system
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9
Q

What is an SIV?

A
  • zoonotic disease that spills over from closely related nonhuman primates
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10
Q

Why are spillover events dangerous?

A

more harmful for new host than the original host species

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11
Q

How does a retrovirus impact protein creation?

A

REVERSE TRANSCRIPTION from RNA of virus –> DNA of host
1. DNA replication of HIV genome
2. DNA transcripts to RNA of HIV genes
3. RNA translates HIV genes to proteins

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12
Q

What is the normal protein creation process?

A
  1. DNA replication
  2. DNA transcripts to RNA
  3. RNA translates to protein
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13
Q

What is AZT?

A

First HIV treatment - almost looks like thymine which blocks the addition of more nucleotides when RNA reverse transcriptase uses AZT instead

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14
Q

How does evolution relate to drug resistance?

A
  • enzymes (like reverse transcriptase) develop proofreading ability
  • many mutations from base sequence error that might make drug resistance or not
  • creates genetic variation where susceptible viruses don’t reproduce and drug-resistant virus reproduce - NATURAL SELECTION
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15
Q

How does mutations affect vaccine development?

A
  • difficult to create a vaccine that is resistant to all possible variants
  • multiple drugs can stop viral infection at different points (when it enters the immune cell, when it replicates, when it leaves)
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16
Q

What is evolution?

A

change in allele frequencies from one generation to the next

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17
Q

What are the principles of NATURAL SELECTION?

A
  • mechanism to explain evolution
  • variation of traits is heritable
  • favoured traits = better survival = higher fitness
  • genotypes with favourable traits become more common

variation (randomly generated) + heritability + non-random survival

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18
Q

What is artificial selection?

A

selective breeding to ensure certain desirable traits appear more in future generations

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19
Q

Why are belief systems contradictory to evolution?

A

Intelligent design: people do no descend from animals
Evolution: species change over time

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20
Q

What is a belief system?

A

relies on beliefs not evidence to form religion

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21
Q

What is scientific theory?

A

testable hypotheses that try to explain facts and are falsifiable

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22
Q

What is a fact?

A

an indisputable observation

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23
Q

What is biogeography of evolution?

A
  • similar species found in distant places
  • common ancestor produced genetic variation over time
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24
Q

What is comparative morphology in macroevolution?

A
  • similar skeletal structure of dissimilar species
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25
Q

What is a vestigial structure?

A

structures that served a purpose for an ancestor but not for the modern ancestor

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26
Q

How does geology prove evolution?

A

earth is billions of years old = plenty of time for slow geological changes

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27
Q

How do fossils prove macroevolution?

A

evidence of extinct forms of life/life on earth was different

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28
Q

What was Darwin’s natural selection theory?

A

descent with modification

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29
Q

Jean-Baptiste Lamarck theory

A

evolution is VARIATIONAL not TRANSFORMATIONAL

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30
Q

What are characteristics evolution?

A
  • GRADUAL
  • cannot be “wanted” or “intentional”
  • every organism doesn’t perfectly suit their environment
  • all species originated from one entity
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31
Q

What is a TRADE OFF?

A

compromise between traits of competing demands (ex. mating vs camoflauge)

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32
Q

How does a zygotes cell cycle compare to a normal cell cycle?

A

switches between interphase and mitosis quickly for higher turnover rate –> single cell to a human

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33
Q

How does a zygotes cell cycle compare to a normal cell cycle?

A

switches between interphase and mitosis quickly for higher turnover rate –> single cell to a human

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34
Q

What is the cell cycle?

A

INTERPHASE: G1, S, G2
MITOSIS: Prophase, Metaphase, Anaphase, Telophase (cytokinesis)

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35
Q

Why do cells divide?

A

multicellular growth, tissue repair, regeneration

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36
Q

What is TURNOVER RATE?

A

frequency of cell moving through cell cycle

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37
Q

Which cells don’t divide? What stage of the cell cycle are they in?

A

neurons –> G0

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38
Q

Why do we have so many cells? Why is cell division important?

A

+ SA:-Volume ratio
- able to satisfy demands faster
- more cell membrane for in/out of cell interactions
- not much loss if one cell dies

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39
Q

What are the stages of Interphase?

A

G1 - cell growth
Synthesis - DNA replication by chromosomal protein duplication
G2 - cell prepares for division

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40
Q

What are cell cycle checkpoints?

A

internal control that prevents a cell from continuing to the next phase before it is ready

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41
Q

What is the G1/S checkpoint?

A
  • determines if cell is ready to divide
  • stops damaged DNA
  • checks if the size is big enough
  • checks for mutations that need to be fixed
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42
Q

What is the G2/M checkpoint?

A
  • commits a cell to mitosis
  • stops DNA if replication error from S
  • checks for mutation/DNA damage
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43
Q

What is the MITOTIC SPINDLE CHECKPOINT?

A
  • before metaphase
  • are chromosomes properly attached to mitotic spindle for proper alignment at metaphase plate
  • influences correct separation at anaphase
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44
Q

What are POSITIVE REGULATORS?

A

promotes movement to the next cell cycle step (CDKs)

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45
Q

How do CDKs and CYCLINS work?

A
  1. Cyclin binds with CDK and gets activated
  2. Phosphate donating protein phosphorylates complex
  3. Complex is activated
  4. Complex phosphorylates target protein
  5. target protein activated
  6. Signals cell to move to the next stage
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46
Q

What is a CYCLIN?

A

protein that regulates CDK activity - 4 types for different stages of cell cycle

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47
Q

What is a CDK?

A

cyclin-dependent kinase; protein that is a positive regulator

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48
Q

What is phosphorylation?

A

Donating a phosphate group

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49
Q

When are cyclins PRESENT? ACTIVATED? DEACTIVATED?

A
  • when in CDK complex
  • always present
  • deactivate when cyclins are degraded
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50
Q

When are CDKs PRESENT? ACTIVATED? DEACTIVATED?

A
  • present only when needed for complex
  • activated in complex
  • degraded when unnecessary
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51
Q

What are NEGATIVE REGULATORS?

A

proteins that stop the cell cycle

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52
Q

What is APOPTOSIS?

A

cell self-destruction when the cell cannot fix itself

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53
Q

What is p53?

A

important negative regulator

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54
Q

How does p53 work?

A
  1. detects DNA damage
  2. Binds to p21 promotor to increase p21 production
  3. p21 is a cyclin-CDK inhibitor
  4. CDK-cyclin complex cannot phosphorylate target protein (cell cycle arrest)
  5. Sends repair enzyme to DNA damage
  6. If repaired positive regulation stimulated – if not repaired apoptosis
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55
Q

What happens when p53 is mutated?

A
  • cell doesn’t get repaired or have apoptosis (no cell cell arrest)
  • leads to cancer
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56
Q

What is PLOIDY?

A

the number of chromosome SETS a species has

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57
Q

What is a DIPLOID?

A

TWO copies of EACH type of chromosome; TWO SETS

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58
Q

What is a HAPLOID?

A

ONE copy of EACH type of chromosome; ONE SET

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59
Q

What is a CHROMOSOME?

A

the nuclear unit of genetic information consisting of a DNA molecule and associated protein

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60
Q

What are SISTER CHROMATIDS?

A

TWO IDENTICAL COPIES of a chromosome held together by a centromere; created during S Phase

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61
Q

What are COHESINS?

A

Proteins that HOLD sister chromatids together; removed during mitosis

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62
Q

What is ANEUPLOIDY?

A

ABNORMAL number of chromosomes AFTER ANAPHASE

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63
Q

What is NONDISJUNCTION?

A
  • Both chromosomes connect to the same spindle in anaphase I or anaphase II
  • one pole gets BOTH chromosomes the other get NONE
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64
Q

MEIOSIS I vs. MEIOSIS II

A

MEOSIS I:
- reductional
(diploid - 2n –> haploid - n)
(4 chromosomes –> 2 chromosomes)
- interphase

MEIOSIS II:
- equational
(haploid –> haploid)
(2 chromosomes –> 1 sister chromatid from each)
- no interphase

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65
Q

Why is there no Interphase before Meiosis II?

A
  • policy must change from meiosis I to meiosis II, so no need for S phase
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66
Q

What is RECOMBINATION?

A
  1. During prophase I, homologous pairs stack on top of each other and homologous CHROMATID exchange any number of segments at the chiasma
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67
Q

What are LINKED GENES?

A

genes that are more likely to get inherited together on a chromatid because their loci are located closer together

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68
Q

What is INDEPENDENT ASSORTMENT?

A

chromosomes at the metaphase plate are segregated to daughter cells independently of each other in metaphase I & II

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69
Q

What is RANDOM FERTILIZATION?

A

two parents bring different genomes and unite to make a unique zygote

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70
Q

How does the zygote form?

A

Haploid sperm fertilizes haploid oocyte = diploid zygote

71
Q

What is chromosome segregation?

A

daughter chromosomes are equally distributed to daughter cells

72
Q

Where does GENETIC VARIABILITY occur in meiosis?

A
  1. recombination
  2. independent assortment
  3. random fertilization

**all by chance/random

73
Q

MITOSIS vs. MEIOSIS

A

MITOSIS:
- one division
- two identical daughter cells
- ploidy remains diploid

MEIOSIS:
- two divisions
- four different daughter cells
- ploidy changes from diploid to haploid

74
Q

What us a KARYOTYPE?

A

number of chromosomes condensed from nucleus and arranged from biggest to smallest

**at metaphase = 2x the number of chromosomes

75
Q

What is Down syndrome?

A

Trisomy 21 (extra chromosome 21)

76
Q

Examples of NONDISJUNCTION of X/Y chromosomes?

A

Turner: no X, only Y
Kleinfelder: XXY (difficult to detect
Triple X syndrome
Super male: XYY
**may be severe or normal

77
Q

Why characterize the genome?

A
  • quantify the genome
  • comparison between species
  • insight into evolution, function, and complexity of an organism
78
Q

What is a GENOME?

A

all of the DNA sequence in one copy of an organism’s chromosome

79
Q

What is the n-value? What is the COEFFICIENT of N?

A

n-value: number of UNIQUE chromosomes (how many chromosomes in each set) - never changes

coefficient of n: number of SETS of chromosomes (ploidy) - changes after synthesis

80
Q

What is the c-value? What is the COEFFICIENT of C?

A

c-value: AMOUNT of DNA in quantity of base pairs or mass (pm) in ONE SET

coefficient of c: how many times the entire genome is present in a cell - number of sister chromatids)

81
Q

What is the relationship between n and c?

A

There is none!

82
Q

What are the main parts of DNA structure?

A

Nitrogenous bases
Deoxyribose sugar-phosphate backbone

83
Q

What does the backbone of DNA look like?

A

Anti parallel strands causes polarity. One is 5’-3’ with a free hydroxyl group and the other is 3’-5’ with a free phosphate.

5-carbon deoxyribose sugar and phosphodiester bond links 3’ to 5’ carbons

84
Q

What are the hydrogenous bases?

A

Adenine-Thymine have two hydrogen bonds

Cytosine-Guanine have three hydrogen bonds

85
Q

How does DNA unwind?

A

Semi conservative

86
Q

What are PURINES? What are PYRIMIDINES?

A

Purine: double ringed - A&G

Pyrimidines: single ringed - T&C

87
Q

DNA REPLICATION

A
  1. Helicase unwinds hydrogen bonds and topoisomerase relieves tension and prevents supercoiling
  2. RNA primer attaches to 3’ end
  3. DNA polymerase III adds deoxiribonucleoside triphosphate with matching base
  4. Sliding clamp encircles DNA binding DNA polymerase to template strand
  5. Ligase seals gaps in lagging strand fragments on 3’ end
  6. DNA polymerase I (exonuclease) replaces RNA primer with DNA
  7. Telomerase extends the new 3’ end
88
Q

What are the LEADING and LAGGING strands?

A

Leading: runs 3’ to 5’
–> new strand is 5’ to 3’

Lagging: runs 5’ to 3’
–> new strand is 3’ to 5’
–> builds in OKAZAKI FRAGMENTS

89
Q

What is the Hayflick limit?

A

the number of times a cell divides before p53 protein signals cell senescence

90
Q

What is cell senescence?

A

cell reacts irreversible cell cycle arrest - G0 - because there are no more telomeres

91
Q

What is a replication bubble?

A

Two replication forks; many bubbles can start simultaneously to increase efficiency for large eukaryotes

92
Q

What is a TELOMERE?

A

non-coding sequence of DNA that buffers the end of chromosome so that DNA is not lost

93
Q

What causes cell senescence?

A

When telomeres become too short after many divisions

94
Q

Where is Telomerase active?

A
  • embryo
  • stem cells
  • white blood cell
  • male germ cell
95
Q

What happens when telomerase is reactivated?

A

cancerous cells – unlimited cell division

96
Q

TELOMERASE PROCESS

A
  1. Single stranded region left on template strand after primer removal
  2. Telomerase binds to 3’ end of single strand and adds more RNA primer
  3. Telomerase shifts and synthesizes more new telomerase DNA
  4. Telomerase leaves the extended template strand
  5. RNA primer added by primase
  6. DNA polymerase III matches base pairs
  7. 5’ end is extended and a short single stranded region remains after primer removal
97
Q

How is SAMENESS inherited?

A
  • complementary base pairs
  • DNA synthesis relies on template strand
  • exonuclease activity of DNA polymerase III PROOFREADS
98
Q

What are sources of DNA DAMAGE?

A

EXOGENOUS: outside cell
–> radioactivity, chemicals, UV light

ENDOGENOUS: inside cell
–> mitochondria, DNA replication, unstable electrons

99
Q

DNA DAMAGE vs MUTATION

A
  • DNA damage: single strand change
  • Mutation: double strand change
100
Q

What are the steps to repair DNA DAMAGE?

A
  1. Proofreading - immediate
  2. Mismatch repair - checkpoint
  3. Excision repair
101
Q

How does PROOFREADING work?

A

DNA polymerase III reverses and uses 3’-5’ exonuclease to remove mismatched pair

102
Q

How does MISMATCH REPAIR work?

A
  1. Repair protein scans and cleaves backbone on each end of the mismatch taking several bases
  2. Gap is filled by repair DNA polymerase
  3. DNA ligase fills gap on 3’ end
103
Q

How does BASE EXCISION REPAIR work?

A

Non bulky DNA damage is recognized and removed by specific protein. DNA polymerase and Ligase replace and seal DNA strand

104
Q

What are THYMINE DIMERS?

A

adjacent thymine crease bulky distortion of backbone stopping DNA polymerase
–> not a mismatch
–> caused by UV light
–> repaired by excision repair

105
Q

How are REACTIVE OXYGEN SPECIES created?

A

Ionizing radiation split water molecules apart creating free radicals that travel unpaired

106
Q

Why are ROS dangerous?

A

highly electronegative and unstable so it will damage DNA to reach stability
–> want to be paired electrons so they pair with proteins (impacting function) RNA or DNA (cut backbone and gets electron from phosphate group)

107
Q

What is the OXYGEN PARADOX?

A

oxygen necessary for survival but its free radicals come from UV radiation, small, diet, toxins. Free radicals cause damage protein in the mitochondria and detoxification proteins get overwhelmed

108
Q

How are DOUBLE STRAND BREAKS repaired?

A

Non-Homologous End Joining - cell in panic state, tries to piece DNA together without template and might cause mutation in DNA.
- deletion
- insertion
- inversion
- return to normal sequence

109
Q

What causes DOUBLE STRAND BREAKS

A

radiation!

110
Q

How much of the DNA sequence is essential?

A

10% - 2% is coding
- the rest is transposons, unknown, introns, or unnecessary

111
Q

What are types of POINT MUTATION?

A

Silent, Nonsense, Missense

112
Q

What is a SILENT MUTATION?

A
  • type of point mutation
  • change in base makes a different codon that codes for the same amino acid = no difference to protein
113
Q

What is a NONSENSE MUTATION?

A
  • type of point mutation
    -change in base makes a stop codon = shorter polypeptide
114
Q

What is a MISSENSE MUTATION?

A
  • type of point mutation
  • change in base makes change in amino acid (might be no difference to significant difference)
115
Q

What are SINGLE NUCLEOTIDE POLYMORPHISMS?

A
  • single nucleotide difference in DNA sequence
  • common type of genetic variation among people
  • used for prediction of health issues
  • most have no affect
116
Q

What happens during DNA polymerase SLIPPAGE?

A

Backwards: insertion of the same sequence = one longer strand

Forwards: skips sequence = one shorter strand

117
Q

What is TAUTOMERIZATION?

A

base shifts to its tautomer form and changes its preferential base pair, causing DNA DAMAGE or MUTATION in future replications

+ base pairing with preferential base is NOT damage

118
Q

What are TRANSITION mutations? What are TRANSVERSION mutations?

A

Transition: purine -> purine or pyrimidine -> pyrimidine

Transversion: pyrimidine -> purine or purine -> pyrimidine

119
Q

What are TRANSPOSABLE ELEMENTS?

A
  • genes that can jump from one loci in the genome to another
  • usually to introns (non coding regions) but it can jump to coding regions
120
Q

What to TEs cause?

A
  • increased genome size
  • effect varies from negligible to disease
121
Q

How have TEs evolved?

A

active TEs insert into safe havens in the genome, but most TEs are inactive due to mutation

122
Q

What happens when TE lands in a protein-coding gene?

A
  • disease causing mutation
  • when excising, it might take a piece of the genome with in and add it to a different section, under a different promoter
123
Q

What was the Blending Theory of Inheritance?

A

1800s - offspring have characteristics of both parents, so offspring must be a blend of the parent generation

124
Q

What were Mendel’s conclusions?

A
  • variation in traits in due to different alleles
  • alleles segregate randomly into gametes
  • organisms inherit two alleles for each trait
  • appearance of heterozygotes is determined by dominant alleles
125
Q

What is the OCA2 gene?

A

gene coding for P protein a surplus of which produces melanosomes which produce a large amount of melanin to make darker eye colour

126
Q

How are the the alleles in dihybrid crosses assorted?

A

independently of each other

127
Q

What is the ratio of two heterozygous being dihybridly crossed?

A

9:3:3:1

128
Q

What is Incomplete dominance?

A

alleles produce intermediate expression

129
Q

How is Tay Sachs Disease an example of incomplete dominance?

A

No Tay Sachs = homozygous dominant = HEX A enzyme produced = fatty structures broken down properly

Mild Tay Sachs = heterozygous = some HEX A enzyme produced = some fatty structures broken down

Severe Tay Sachs = homozygous recessive = no HEX A = no fatty structures broken down

130
Q

What is Codominance?

A

alleles are EQUALLY expressed in heterozygotes

131
Q

How is Blood Type an example of Codominance?

A

Type AB has equally expressed type A and type B

Type A: Antigen A on RBC and Anti-B antibody in plasma

Type B: Antigen B on RBC and Anti-A antibody in plasma

Type AB: Antigens A+B

Type O: Anti-A and Anti-B antibodies

132
Q

What happens in incompatible blood transfusion?

A

surface antigens and opposing antibodies cause haemolysis (destruction of RBC)

133
Q

What are glycoproteins? How do they relate to blood type?

A
  • found on RBC membrane made of sugars, the terminal of which determines which antigen and therefore blood type
  • terminal sugar is added by glycotransferase which are different for each blood type

(Type O is nonfunctional glycotransferase)

134
Q

How do sex-linked characteristic differ in males and females?

A

different inheritance patterns – males have a higher chance because they only need one while females can be a carrier

135
Q

How does autosomal recessive disorders compare with sex-linked disorders?

A

autosomal-males can be carriers
higher chance of sex-linked disorders

136
Q

What is a polygenic trait?

A

continuous variation in a population of a phenotype because there are so many genes involved (fur/skin)

137
Q

What is an epistatic gene?

A

Interferes with gene expression

138
Q

Why was the blending theory not plausible?

A

–> “factors” are always intermediate
–> doesn’t explain evolution of traits (how genes can skip a generation)

139
Q

How did Mendel use the scientific method?

A
  • pea plant experiment
  • controlled test crosses (rr with dominant phenotype)
  • observable analysis
  • high reproduction rate
140
Q

How is epistasis different from Mendelian genetics?

A

epistasis: the genes expressed can be masked by another gene in a continuum (9:3:4)

Mendelian genetics is dominant masks the recessive for a single gene (9:3:3:1)

141
Q

What is microevolution?

A

changes in allele frequencies that occur form one generation to the next

142
Q

What is macroevolution?

A

large scale evolutionary patterns

143
Q

How can you calculate observed phenotype frequency?

A

sum of species with the phenotype/total population (total phenotype frequency should add to 1)

144
Q

How can you calculate observed genotype frequency?

A

of species with the genotype/total population

145
Q

How can you calculate observed allele frequency?

A

total number of one allele type/total number of alleles

if there is 36 BB, then 72 alleles
if there is 100 in population, there is 200 alleles

146
Q

What is the Hardy Weinberg Principle?

A

no evolutionary agents and random mating

expected frequencies = observed frequencies

allele frequencies DO NOT change over generations, no evolution at that locus

147
Q

How can you calculate expected genotype frequency (no EA and random mating)?

A

p^2 – BB

2pq – BR

q^2 – RR

where p and q are the allele frequencies

148
Q

What are evolutionary agents?

A
  • selection
  • mutation
  • immigration/migration
  • genetic drift
149
Q

What is fitness?

A

contribution of offspring (of their alleles) to future generations
–> fitness depends on how many offspring is being produced by others of the same species

150
Q

What is absolute fitness?

A

of offspring that survive to reproductive age

151
Q

What is relative fitness?

A

compare absolute fitness to the maximum fitness in the species:

absolute fitness/absolute fitness of the most successful genotype

152
Q

What is genotypic fixation?

A

100% frequency of a genotype

153
Q

Selection against the dominant phenotype?

A

BB = BR < RR
–> frequency of B allele, BB, and BR genotypes would reach 0
–> frequency of R allele and RR phenotype would reach 100 (fixation)

154
Q

Selection against recessive phenotype?

A

BB = BR > RR
–> BR doesn’t allow for fixation (R allele is still present)
–> dominant allele reaches a high value - not 100%

–> frequency of recessive would reach >0%

155
Q

Is it possible to completely remove recessive phenotypes?

A

No – selection acts of phenotypes, so recessive genotype can hide in heterozygous genes

156
Q

What is a distribution of phenotypes?

A

range of phenotypes from many alleles/loci (ex. height)

157
Q

Selection in a distribution of phenotypes?

A

–> reduces genetic diversity
–> result in DIRECTIONAL selection, shifting towards one end of the distribution

158
Q

What is heterozygous advantage?

A

SS < NS > NN
–> codominance and incomplete dominance only

159
Q

What is stabilizing selection?

A

result of heterozygous advantage
–> mean phenotype favoured

160
Q

What is heterozygous disadvantage?

A

WW > WS < SS
–> codominance and incomplete dominance only

161
Q

Why does starting allele frequency matter in heterozygous disadvantage?

A

the one that is more common to start will reach fixation

rare allele will decrease and might disappear because the rare alleles will most likely be found in heterozygotes

162
Q

What is the affect of heterozygous advantage on diversity?

A

increases genetic variation –> common alleles become less common, rare alleles become more common, and extreme alleles possible
–> no fixation

163
Q

What is the affect of heterozygous disadvantage on diversity?

A

decreases genetic variation –> more common allele becomes more common

164
Q

What is disruptive selection? What does it cause?

A

extreme phenotypes favoured so the two extremes can evolve to two different populations

165
Q

What is gene flow?

A

any movement of individuals or genetic material from one population to another (immigration and emigration)

166
Q

What is genetic drift?

A

by chance not all alleles of parents is passed to offspring, occurring as long as the population is not infinitely large
–> rare alleles more likely to be lost
–> greater impact on smaller populations
–> reduces genetic variation

167
Q

What is the bottleneck effect?

A

change in allele frequency due to random sampling of a very small number of individuals due to large reduction in population
–> reduction of diversity

168
Q

What is the founder effect?

A

population reduction is due to a small number of individuals starting a new population
–> loss of alleles by chance

169
Q

What is assortative mating?

A

mating between similar phenotypes
–> increases homozygosity
–> if this is across the genome this is INBREEDING

170
Q

What are the consequences of INBREEDING?

A

–> exposes harmful recessive alleles –> inbreeding depression –> health issues

171
Q

What is non random mating?

A

individuals select mate based on phenotype but this doesn’t change allele frequencies, so it is not an evolutionary agent

172
Q

What is disassortative mating?

A

mating with dissimilar phenotypes which increases heterozygosity (inbreeding avoidance aka outcrossing)

173
Q

What is binary fission?

A

asexual reproduction in prokaryotic cell

174
Q

What are the steps of binary fission?

A

B period = bacterial cell birth and growth

C period = circular chromosome replication begins in the middle of the cell and the replicated oris move to opposite poles

D period = replication complete; plasma membrane grows inward and cell wall synthesized

Fall 2022 (12 decks)

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