Exam 3 Flashcards

Question

How does a genomic library differ from a cDNA libray?

Answer 1

* a genomic library is created by inserting fragments of chromosomal DNA into a **_cloning vector._** Chromosomal DNA is randomly fragmented by shearing or by partial digestionwith a restriction enzyme. * a cDNA library is made from **_mRNA_** sequences. Cellular mRNAs are isolated and then reverse transcriptase is used to copy the mRNA sequences to cDNA, which are cloned into plasmid or phage vectors.

Answer 2

is a **_set of clones_** (i.e. bacterial or yeast cells) that collectively **_contain_** an entire **_"set" of DNA_**

Answer 3

1. Genomic libraries (contains all of the DNA sequences found in an organism's genome) 2. cDNA libraries (from mRNA that is first converted into DNA and then cloned into bacteria.)

Answer 4

1. the set of **bacterial colonies** or phages containing all the **DNA fragments** from human cells 2. **Total genome** of an organism. 3. **a lot of gene material** is needed e.g. white blood cells

Answer 5

is created from **mRNA** that is first **converted** into **DNA** and then **cloned** into *_bacteria. _*

Answer 6

1. cells are collected and disrupted which causes them to release their DNA 2. DNA is extracted from solution 3. DNA is cut into fragments by restriction enzymes for LIMITED AMOUNT OF TIME (partial digestion) 4. DNA molecules will be cut in ¥ (different) places 5. set of overlapping fragments are produced 6. fragments are put into vectors 7. vectors are transfered to bacteria. 8. The set of clones contain overlapping genomic fragments, some of which may include segments of the gene of interest.

Answer 7

some clones conain the entire gene of interest, others include part of the gene, and most contain none of the gene of interest.

Answer 8

Restriction enzymes exist naturally in bacteria, which use them to prevent the entry of viral DNA

Answer 9

1. **Organization** and 2. **sequence** of genetic information contained within a genome.

Answer 10

1. **Map** a genome --\> **physical and genetic** maps 2. **Break** the chromosomes _into_ **fragments** 3. **sequence** the fragments (**LIBRARY)** 4. use a computer to **resassemble** the fragment sequences into whole chromosomes sequences.

Answer 11

* recombination * percent recombination * centimorgans

Answer 12

Includes identification of: 1. all **_RNAs_** that are transcribed from a genome 2. all the **_proteins_** that are encoded in the genome, 3. detemination of _what those RNAs and proteins **do**_ in the cell.

Answer 13

Single nucleotide polymorphism

Answer 14

Specific set of SNPs (single nucleotide polymorphism) observed on a single chromosome.

Answer 15

* linked * disease * HapMap (haplotype map)

Answer 16

Seventy genes were identify whose expression patterns accurately predicted the recurrence of breast cancer within 5 years of treatment.

Answer 17

* rely on **_nucleic acid hybridization**_, in which a known _**DNA fragment is_** used as a **_probe_** to find complementary sequences. * can provide information about the expression of thousands of genes --\> this enables us to study **_WHICH GENES ARE ACTIVE_** in particular tissues.

Answer 18

comparisions fo data from different species helps scientists understand how genomes function and evolve.

Answer 19

1. 1/3 2. metabolism

Answer 20

larger genomes.

Answer 21

1. Transcription factors 2. Nucleic acid enzymes.

Answer 22

1. The goal of the HPP would be to assign functions to all of the proteins in the human body, and to undestand how the proteins interact with each other in the cell. 2. Current technology is too SLOW and tedious for protein analysis

Answer 23

1. RNAs are not always just the "middlemen" between DNA and protein. 2. **_many RNAs are the "gene product" and are never translated to make protein at all._** They do their own function in the cell

Answer 24

transcriptome

Answer 25

Genetics is old in the sense that humans have been aware of **_hereditary principles_** for thousands of years and have applied them since the beginning of **agriculture.** It is very young in the sense that the **_fundamental principles_** were not uncovered until **Mendel’s time**, and that the **structure of DNA** and the **principles** of **recombinant DNA** were discovered within the past **60 years**. The use of genetics by humans began with the **_domestication_** of plants and animals. The ancient Greeks developed the concepts of pangenesis and the inheritance of acquired characteristics. Preformationism suggested that a person inherits all of his or her traits from one parent. Blending inheritance proposed that offspring posses a mixture of the parental traits.

Answer 26

**_DNA methylation_** is one way that _genes_ are **turned off** (e.g. they will not be expressed in that cell). The methylation is **kept** throughout subsequent **cell divisions.** That means that the newly synthesized DNA (at the **end of S phase** in the cell cycle) will be methylated in the same places that the parental DNA was methylated. Turning off genes is the main way that a **totipotent stem** cell changes into cell types that are increasingly determined to becoming a certain cell type, until the _cell is fully differentiated._ _**FASD** (fetal alcohol spectrum disorder) or **FAS** (fetal alcohol syndrome) e_ncompasses three broad phenotypes: 1) prenatal and or postnatal **growth retardation;** 2) distinctive **facial features** (short palpebral fissure, smooth philtrum, thin vermillion border of the upper lip); and 3) **brain damage**. Others are cardiac septal defects and minor joint abnormalities.

Answer 27

* Both spermatogenesis and oogenesis **begin** similarly in that the **diploid primordial cells** (_spermatogonia and oogonia)_ can undergo _multiple rounds of mitosis_ to produce more primordial cells, **or** both types of cells can _enter into meiotic division._ * Like spermatogenesis, oogenesis involves the creation of **haploid sex cells** through the process of meiosis * Spermatogenesis: * **_Meiosis I**_ product is _**2 haploid_** secondary spermatocytes * **_Meiosis II_** product is **_4_** **_haploid_** spermatids * Final result of spermatogenesis is **_4 haploid sperm cells_** for each spermatogonia. * Occurs in the male testes. Both **_maturation and divisions_** are completed in testes themselves. * Small amount of **_cytoplasm_** is present * Oogenesis: * **_Meiosis I_** product is **_1 haploid_** secondary oocyte & **_1 polar body_**. * **_Meiosis II**_ is _**1 haploid ovum_** & 1 polar body. * Final result is **_one egg cell and 2 polar bodies_** for each oogonia but only if fertilization has occurred. * Occurs in **_female ovaries_**. First maturation division is completed in the ovaries but the second one is completed outside ovaries after fertilization begins. * Large amount of **_cytoplasm_** is present → providing most of the mitochondria and the cytoplasm for a new fertilized egg.

Answer 28

* Similarities: 1. **5’→3’** (new strand) bidirectional from the origin in bacteria. 2. It is synthesized in the **nucleus.** 3. Involve specific **complementary base pairing** and **unwinding** of the double helix DNA. * Differences DNA replication 1. The initiation point is at the **origin** of replication in DNA 2. The final product is replicated chromosomes **Dyads** → sister chromatids 3. Critical **enzymes**: initiator proteins, helicase, SSBPs, gyrase/topoisomerase, primase, DNA poly III, DNA poly I, ligase. * Differences RNA transcription: 1. The initiation point is at the **promoter** in DNA 2. The final product is **RNAs** (all types). 3. Critical **enzymes**: RNA-polymerase (with a built in helicase)

Answer 29

1. **Uncontrolled growth** 2. Loss of "**contact inhibition**" (or "density-dependent inhibition") --\> "cells cannot tell it is getting too crowded so they keep replicating" 3. **Accumulation** of gene mutations and large chromosomal abnormalities. 4. Ability to **metastasize** (spread to other areas of the body)

Answer 30

1 in 2 | (or maybe as good as 1 in 3)

Answer 31

1. Most cancers are **_sporadic_** (85-95%) as opposed to those with and inhereted component (5-15%) 2. Most cancers result from an **_accumulation**_ of several specific _**gene mutations_** in the same cell, (i.e. the **_multi-step model_** of cancer) 3. Tumors are **_clonal_**, so only one original cell needs to accumulate the mutations in order for a tumor to form

Answer 32

* Is a childhood cancer of the eye. * It is unusual because it is caused by a **_homozygous mutation in a single gene_**

Answer 33

Two-hit hypothesis

Answer 34

Just one cell of the retina needs to accumulate a mutation in the other RB copy, and tumor will form.

Answer 35

then a single cell must accumulate mutations in both copies of the gene to get the cancer --\> **_have 2 sporadic mutations_**

Answer 36

_**early** onset_ and _**bilateral** tumors (both eyes)_

Answer 37

_**later** onset_ and _**unilateral** tumor_ (one eye)

Answer 38

Multi-step progression

Answer 39

1. Genes which encode proteins that STOP the cell cycle (**_Tumor-suppressor genes_**) 2. Genes whic encode proteins which PROMOTE the cell cycle (**_Proto-oncogenes_**)

Answer 40

1. Genes which encode proteins important for **_DNA repair_** (DNA repair genes) Example: Xeroderma pigmentosum) 2. Genes that regulate **_Telomerase_** 3. Genes that promote **_angiogenesis_** 4. Genes that are needed for proper **_cytoskeleton (*palladin* gene) _**or ECM structure 5. Genes which encode proteins that STOP the cell cycle (**_Tumor-suppressor genes_**) 6. Genes whic encode proteins which PROMOTE the cell cycle (**_Proto-oncogenes_**)(proto = first, before) (A proto-oncogene is a non-mutated form of normal cellular gene that control cell growth and it has the potential to become oncogene causing cancer usually after its overexpression. )

Answer 41

* inhibit * recessive * mutated

Answer 42

* _Loss_ of _heterozygosity_ * _tumor suppressor_ gene

Answer 43

1. **_p53:_** transcription factor, regulates apoptosis 2. **_RB (retinoblastoma):_** transcription factor 3. **_WT-1_** Transcription factor (e.g. children's kidney cancer)

Answer 44

1. About **½ of all human cancers** express a mutant p53 (**Tumor suppressor gene**) 2. **Li-Fraumeni Syndrome** -- an inhereted dominant p53 mutation with leads to high occurrences of a wide range of malignancies (risk developing several types of cancer)

Answer 45

The RB protein helps control the progression through the G1/S check point by binding transcription factor E2F 1. RB **bind to EF2** keeps it inactive 2. increasing concentration o**f cyclin-D-CDK** and **cyclin -E-CDK _phosporilates RB_** 3. phosporilation inactivates RB and it is **released** from **E2F** 4. **E2F binds to DNA** and stimulates the transcription of genes required for DNA replication.

Answer 46

* **RB won't be made** * **E2F will always be active** ---\> which binds to DNA and stimulates the transcription of genes required for DNA replication.

Answer 47

1. **Proto-oncogenes** normally produce factors that stimulate **cell division** 2. **Mutant** alleles (**oncogenes)** tend to be **dominant**: one copy of the mutant allele is sufficient to induce excessive cell proliferation.

Answer 48

1/3 ***_ras_*** is a **_Proto-oncogene_**

Answer 49

1. With a reciprocal **_translocation**_ between chromosome 9 and 22 --\> _**philadelphia chromosome_** 2. Chronic myelogenous leukemia (CML)

Answer 50

* Its product is located in the **cell membrane** * Its function is **GTP binding** and **GTPase**

Answer 51

1. Its product is located in the nucleus 2. Its function is transcription factor

Answer 52

1. Translocation of a potential cancer-causing gene to a new location, where it is activated by different regulatory sequences. 2. The c-MYC protein stimulates the division fo the B cells and leads to Burkitt's lymphoma

Answer 53

1. They cause cancer if they **_carry a mutated oncogene_** into the cell --\> mutating and rearranging proto-oncogenes, or 2. if they **_integrate**_ onto a chromosome _**next**_ to a _**proto-oncogene_** (A normal gene that has the potential to become an oncogene. T) --\> remember viruses carry strong promoters

Answer 54

multi-step

Answer 55

1. Loss of normal _tummor suppressor gene **APC**_ --\> a **polyp** (a bening, precancerous tumor grows) * 2 copies need to be lost or mutated to cause cancer (homozygous recessive) 2. Activation of oncogene ***_ras_*** ---\> an **adenoma** (a bening tumor grows) * only 1 copy needed to be mutated or lost to cause cancer. 3. Loss of tumor-suppressor gene **_p53_** --\> a **carcinoma** (s malignant tumor develops) * 2 copies need to lost or mutated to cause cancer. * So far 4 mutations have accumulated 4. Other changes; loss of antimetastasis gene --\> the cancer metastasizes through the bloodstream

Answer 56

1. FAP (familial adenomatous polyposis)--\> APC mutation (loss of normal tumor-suppressor gene APC) 2. HNPCC (hereditary non-polyposis colon cancer) --\> DNA repair mutation. Both result from the same collection of mutations in 1 colon cell, but the gene mutation which is inhereted is different. [APC, p53, ras]

Answer 57

* Large population * Random mating * No significant rate of mutation, migration, or natural selection

Answer 58

a cell surface receptor protein that is necessary for HIV-1 to bind to cells. ## Footnote

Answer 59

The 32-bp deletion in exon 4 of the CCR5 gene, if homozygous, confers resistance to HIV infection. The Greek letter Δ (delta) stands for “deletion.” The CCR5 gene has two alleles of importance to us: * CCR5-1 (normal) * CCR5-Δ32 (mutant)

Answer 60

**Loss** of genetic variation

Answer 61

an equilibrium, with the allelic frequencies being determined by the relative rates of forward and reverse mutation.

Answer 62

An individual belonging to a group of organisms (or the entire group itself) having **common characteristics** and (usually) are capable of **mating** with one another to produce **fertile offspring**

Answer 63

New mutations **change allelic frequencies**, but eventually the rate of _forward and reverse mutations_ will **reach equilibrium**

Answer 64

Migration will **_affec_**t a population’s _gene pool_ if the number of **migrating** individuals is **significant** and if the **allele frequencies** are quite **different.**

Answer 65

**Genetic drift**: large changes in allele frequencies in a short period of time. ## Footnote Small populations are much more likely to experience genetic drift than large populations.

Answer 66

* Common in **_CML (Chronic Myelogenous Leukemia)_** , this translocation creates a **_fusion protein_** that is overactive. * **Reciprocal translocation** between Chromosome **9 and 22** (Philadelphia Chromosome) causes CML (Chronic Myelogenous Leukemia)

Answer 67

* Although many genes contribute to coat color and pattern in domestic cats, a single **X-linked** **_locus_** determines the presence of **orange color**. There are two possible alleles at this locus: **X+,** which produces non-orange (**usually black) fur**, and, **Xo,** which produces **orange fur**. _Males_ are **_hemizygous_** and thus may be black (X+Y) or orange (XoY) but not black and orange. * _Females_ may have the tortoiseshell (X+Xo) pattern arising from a **patchy mixture** of black and orange fur. Each **orange patch** is a **clone of cells** derived from an original cell in which the _black_ allele is _inactivated_ (Barr body) and each **black patch** is a **clone of cells** derived from an original cell in which the _orange_ allele is _inactivated **(Barr body)**_.

Answer 68

Use ***h*** for the **recessive hairless** allele and ***H*** for the **dominant allele** for the presence of **hair**. Because H is dominant over h, a rat terrier with hair could be either **homozygous (HH)** or **heterozygous (Hh)**. To determine which genotype is present in the rat terrier with hair, **cross** this dog **_with a hairless rat terrier (hh)._** If the terrier with hair is **homozygous (HH),** then **no hairless offspring** will be produced by the test cross. However, if the terrier is **heterozygous (Hh)**, then **½ of the offspring will be hairless.**

Answer 69

Hfr x F- = Hfr + F- (no change) 1. In order to get an Hfr I need to **conjugate F+ with an F- first.** Then the F factor (produces the **sex pili)** is **integrated** into the bacterial chromosome in the F- cells. This takes place with cross over between the F factor and the chromosome. 2. When this plasmid with the sex pili is part of the bacterial chromosome we get the **Hfr.** 3. Then this bacteria is **expressing the gene for the pili** which can then use it to **donate DNA to an F-** bacteria by using the ***_rolling over or unidirectional copying_***. But the chromosome is now too long and the _cells won’t stay attach_ through the pili in order to transmit the whole chromosome. 4. So the **transmission is halted** and only a section of the chromosome is transferred to the F-. Which can contain _only part of the pili sex genes and another **mutant gene.**_ 5. The transfer **strand replicates** → then 1) **restriction enzymes** can degrade the new strand or 2) **crossing over** can take place between the donated Hfr chromosome and the original chromosome of the F- cell. 6. This crossing over leads to the **recombination of alleles** and F- cell contains the mutant allele while the rest of the **linear chromosome is degraded**.

Answer 70

* The Bombay phenotype **suppresses** the expression of alleles at the **ABO locus.** In most people, a dominant allele (H) encodes an enzyme that makes H, a molecule necessary for the production of antigens. * People with the Bombay phenotype are **homozygous** for a **recessive mutation (*h*)** that encodes a _defective enzyme._ * The **defective enzyme** is incapable of making H and, because **H is not produced**, **_NO ABO antigens are synthesized._** * People with genotype ***hh,*** who would normally have A, B, or AB blood types, **do not produce antigens** and therefore **express an O phenotype**. In this example, the alleles at the **ABO locus are hypostatic** to the recessive h allele. The gene that does the masking is called an **epistatic gene.**

Answer 71

* For some genes, having an extra copy may not cause any detectable problem. For others though, it can upset the carefully regulated interactions inside the cell, and create a problem. * This drastic phenotypic effects are due to that gene products from the extra chromosome or individual genes alter the delicate regulated interactions among gene products inside the cell and among cells. * **_Pateau Syndrome_** which has an extra copy of **chromosome 13 ** (**_47, XX or XY, +13)_** will cause more genetic material from this chromosome to produce more proteins responsible for appropriate heart muscle development and neural tube or the roof of the palate. This in turn will create ventricular septal defect, or neural tube defects, cleft palate and other defects. This imbalance in **trisomy 13** leads to too many defects for a baby to live past 3 days. Very rare cases make it to 6 months.

Answer 72

* Blobel postulated (then demonstrated) that proteins secreted out of the cell contain an **_intrinsic signal_** that governs them to and across membranes and allows for their localization in the correct location of the cell. * The idea that **secretory proteins** are synthesized with an **amino terminal extension** that is recognized by a **cytosolic factor** and that, _together,_ they are responsible for targeting to the **endoplasmic reticulum.**

Answer 73

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that causes muscle weakness, disability and eventually death. ALS is inherited in most cases in an autosomal dominant pattern. Many patients would consider assisted suicide. The disease severity, treatment ineffectiveness and increasing dependence on caregivers give rise to thoughts to terminate life among patients, especially those at an advance stage. In ALS1, mutation in the Cu-Zn Superoxide Dismutase 1 gene (SOD1) on chromosome 21q22.1 correlates with the ALS phenotype. SOD1 is an enzyme that catalyzes the destruction of O2- free radicals, thus conferring protection to cells from the harmful effects of superoxide free radicals. The mutations in the SOD1 gene are thought to be pathogenic through a gain in toxic property (e.g. by misfolding and aggregation) rather than a loss of function of the protein. Disease duration or rate of disease progression does correlate with some mutations. Particularly the A4V mutation (Deng, 1998) causes about 50% of ALS1 in North America families being consistently associated with a rapid course from symptoms onset until death. This is a missense mutation where a single base pair substitution results in the translation of a different amino acid at that position. The amino acid alanine is replaced by valine in the genetic code, introducing an incorrect amino acid into the protein sequence. Another mutation is I113T, which also occurs at the SOD1 dimer interface. These mutations exhibited reduced superoxide scavenging ability due to misfolding of the homo-dimer at the interface. Currently there are two hypothesis that describe the mechanism by which mutations in SOD1 causes familial ALS. The oligomerization hypothesis, in which normally soluble, functional proteins misfold to form some toxic multimeric species. These aggregated proteins can be also bind to other essential proteins inside the neurons making them unavailable to perform their function. The second hypothesis is the oxidative damage where mutant CuZnSOD proteins are mutated at the metal-binding regions. This mutant CuZnSOD catalyzes reactions with hydrogen peroxide that damages important substrates for cell survival. In summary oligomerization in CuZnSOD proteins seem to be a very important explanation for the toxicity of these proteins in the neurons in patients with ALS. The upper motor neurons and the lower motor neurons degenerate or eventually die, and stop sending messages to muscles. Unable to function, the muscles gradually weaken and atrophy.

Answer 74

* Discovered that "R" bacteria could become deadly simply when combined with inert lethal "S" form in a test tube—the mice were unnecessary to the equation. * They, like Griffith, attempted to transform the R strain into the S strain by incubating living R and heat-killed S. They pre-treated the heat-killed bacteria (S strain) by making 3 samples one with RNase (destroys RNA), the second with Protease (destroys proteins) and the third one with DNase (destroys DNA). * Then they mixed the 3 samples with R strain and got the following * 1st R strain + RNas = Type R and type S * 2nd R strain + Protease = Type R and type S * 3rd R strain + DNase = Type R only * They concluded that DNA was the transforming susbtance --\> Genetic information resides in DNA

Answer 75

* In their experiments, they used two radioactive markers to label the proteins and the DNA of the phages. The proteins were labeled with 35S (a radioactive form of sulfur) and the DNA was labeled with 32P, a radioactive form of phosphorus. This allowed the researchers to easily differentiate between a sample that contained protein (thus would have 35S present) and a sample that only contained DNA (thus would have 32P present). * During a phage infection, it was hypothesized that some part of the phage was injected into the bacterium and it was this injected material that conveyed the genetic material necessary to produce new phages. Hershey and Chase determined that the phage injected only the DNA into the bacterium and concluded that DNA must be the genetic material in phages. * This was done by a series of two experiments in which different sets of non-radioactive bacteria were incubated with phages that had either their protein or their DNA labeled (as described above). * They allowed the phages to infect the bacteria for a short time, they agitated the incubations to dislodge any loose parts of the phages. * The bacteria cells were then pelleted (sedimentar) in a centrifuge and the location of the radioactivity. They found that the radioactive DNA was always found with the bacteria cells and that the radioactive protein was always in the supernatant. This suggested that the DNA was injected into the bacteria but the protein coat was not. Thus all of the information needed to produce new viruses was contained in the DNA and not the protein.

Answer 76

1. Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that causes muscle weakness, disability and eventually death. ALS is inherited in most cases in an autosomal dominant pattern. Many patients would consider assisted suicide. 2. The disease severity, treatment ineffectiveness and increasing dependence on caregivers give rise to thoughts to terminate life among patients, especially those at an advance stage. 3. In ALS1, mutation in the Cu-Zn Superoxide Dismutase 1 gene (SOD1) on chromosome **_21q22.1_** correlates with the ALS phenotype. SOD1 is an enzyme that catalyzes the destruction of O2- free radicals, thus conferring protection to cells from the harmful effects of superoxide free radicals. The mutations in the SOD1 gene are thought to be pathogenic through a gain in toxic property (e.g. by misfolding and aggregation) rather than a loss of function of the protein. 4. Disease duration or rate of disease progression does correlate with some mutations. Particularly the **_A4V**_ mutation (Deng, 1998) causes about 50% of ALS1 in North America families being consistently associated with a rapid course from symptoms onset until death. This is a missense mutation where a single base pair substitution results in the translation of a different amino acid at that position. _**The amino acid alanine is replaced by valine_** in the genetic code, introducing an incorrect amino acid into the protein sequence. 5. Another mutation is **_I113T (_****_substitution of the amino-acid Isoleucine 113_****_to the amino-acid threonine)**_, which also occurs at the SOD1 dimer interface. These mutations exhibited reduced superoxide scavenging ability due to_**misfolding of the homo-dimer at the interface._** 6. Currently there are two hypothesis that describe the mechanism by which mutations in SOD1 causes familial ALS. 7. The oligomerization hypothesis, in which normally soluble, functional proteins misfold to form some toxic multimeric species. These aggregated proteins can be also bind to other essential proteins inside the neurons making them unavailable to perform their function. 8. The second hypothesis is the oxidative damage where mutant CuZnSOD proteins are mutated at the metal-binding regions. This mutant CuZnSOD catalyzes reactions with hydrogen peroxide that damages important substrates for cell survival. 9. In summary oligomerization in CuZnSOD proteins seem to be a very important explanation for the toxicity of these proteins in the neurons in patients with ALS. The upper motor neurons and the lower motor neurons degenerate or eventually die, and stop sending messages to muscles. Unable to function, the muscles gradually weaken and atrophy.

Answer 77

The linear sequence of amino acids (stabilized by peptide bonds between adjacent amino acids)

Answer 78

The alpha helix and beta-pleated sheet (stabilized by hydrogen bonds between backbone atoms of non-adjacent amino acids; no R groups are involved in bonding at the level)

Answer 79

The 3D shape (bonding is between R groups of nonadjacent amino acids; involves disulfide bridges between cysteine residues, ionic or salt bridges, hydrogen bonds, hydrophobic interactions)

Answer 80

Involves more than one polypeptide chain serving as subunits in a larger complex (all bond types may be involved:. Not all proteins have a quaternary structure.

Answer 81

Globular or fibrous

Answer 82

Is evolution within a lineage with the passage of time.

Answer 83

Is the splitting of one lineage into two

Answer 84

natural selection

Answer 85

1) Prezygotic * Ecological: differences in habitat; individuals do not meet * Temporal: reproduction takes place at different times * Mechanical: anatomical differences prevent copulation * Behavioral: differences is mating behavior prevent mating * Gametic: gametes incompatible or not attracted to each other. 2) Postzygotic * Hybrid inviability: hybrid zygote does not survive to reproduction * Hybrid sterility: hybrid is sterile * Hybrid breakdown: F1 hybrids are viable and fertil, but F2 are inviable or steril.

Answer 86

* speciation by geographic isolation, * Isolation might occur because of great distance or a physical barrier, such as a desert or river * In order for a speciation even to be considered “allopatric,” gene flow between the soon-to-be species must be greatly reduced—but it doesn’t have to be reduced completely to zero.

Answer 87

* Arises when reproductive isolation existe in the absece of any geographic barrier.

Answer 88

depict evolutionary relationships based on current data

Answer 89

The evolutionary relationship among a group of organisms

Answer 90

“silent mutations”

Answer 91

Phylogenetic trees

Answer 92

* Proto- Oncogene 1. **ras:** (1/3 of all tumors have a ras mutation). Located in cell membrane. Function: GTP binding and GTPase. 2. **myc:** Located in nucleus. Function: transcription factor * Tumor-suppressor genes 1. **p53:** (1/2 of all tumors have a p53 mutation**)** transcription factor, regulates apoptosis 2. **RB (**retinoblastoma): transcription factor 3. **WT-1** Transcription factor (e.g. children's kidney cancer)

Exam 3 Flashcards

(122 cards)