AP Bio: Viruses and Molecular Biology of Cancer – Flashcards

Mutations in the genes that normally regulate cell growth and division in somatic cells can lead to cancer.

a gene found in viral or cellular genomes that is involved in triggering molecular events that can lead to cancer

a normal cellular gene that has the potential to become an oncogene

1. point mutations in proto-oncogenes that result in a constitutionally active protein product 2. localized reduplication (gene amplification) of a DNA segment that includes a proto-oncogene, leading to overexpression of the encoded protein 3. chromosomal translocation that brings a growth-regulatory gene under the control of a different promoter and that causes inappropriate expression of the gene

p53 acts in several ways to prevent a cell from passing on mutations due to DNA damage. If mutations do accumulate and the cell survives through many divisions—as is more likely if the p53 tumor-suppressor gene is defective or missing—cancer may ensue

-Changes in a tumor parallel a series of genetic changes, including mutations affecting several tumor-suppressor genes (such as p53) the ras proto-oncogene. -Mutations of tumor-suppressor genes often entail loss (deletion) of the gene. Other mutation sequences can also lead to colorectal cancer.

-Adolf Mayer was researching tobacco mosaic disease. He discovered the disease must be excedingly small for it to be transmitted by tree sap. -Martinus Beijerinck ruled out the possibility that the disease was due to a filterable toxin produced by a bacterium by demonstrating that the infectious agent could reproduce. -Wendell Stanley crystallized the pathogen, the tobacco mosaic virus (TMV) -Dmitri Ivanowsky was the first man to discover viruses

- capsid built from capsomeres encloses the viral genome - some viruses have accessory structures to help them infect their hosts - membranous envelope surrounds the capsids of flu viruses - elongated icosahedral capsid heads and protein tail pieces are on t-even phages

can only reproduce within host cells because they lack metabolic enzymes, ribosomes, and other equipment for making proteins

-The virus recognizes its host cell by the "lock and key" --between proteins on the outside of the virus and specific receptor molecules on the host's surface

while phages have the potential to wipe out a bacterial colony in just hours, bacteria have defenses against phages - natural selection favors bacterial mutants with receptor sites that are no longer recognized by a particular type of phage - bacteria produce restriction enzymes that recognize and cut up foreign DNA, including certain phage DNA - their activity restricts the ability of the phage to infect the bacterium - chemical modifications to the bacteria's own DNA prevent its destruction by restriction enzymes

-lytic cycles: destroys the host -lysogenic cycles: phage genome replicates without destroying the host cells

-glycoproteins on the envelope bind to specific receptors on the host's membrane - envelope fuses with the host's membrane, transporting the capsid and the viral genome inside - (if it has an RNA genome) viral glycoproteins for new envelopes are made by ribosomes bound to the ER of the host cell - viral glycoproteins are then glycosylated by cellular enzymes in the ER and Golgi apparatus - these glycoproteins are transported to the cell surface, where they wrap themselves in membrane as they bud from the cell

- HIV enters the host cell, reverse transcriptase molecules are released into the cytoplasm and catalyze the synthesis of viral DNA - newly made viral DNA enters the cell's nucleus and is inserted as a permanent provirus into a chromosome - host's RNA polymerase transcribes the proviral DNA into RNA molecules that can function both as mRNA for the synthesis of viral proteins and as genomes for new virus particles released from the cell

Both evolve by natural selection, respond to the environment, and grow. Although these are true, viruses aren't living organisms because they aren't made of cells nor can reproduce independently.

most molecular biologists favor the hypothesis that the earliest viruses were naked bits of nucleic acids that passed between cells via injured cell surfaces - evolution of capsid genes may have facilitated the infection of undamaged cells

a type of DNA that can move around within the genome: plasmids, transposons and viruses.

Viral infections can cause the release of hydrolytic enzymes from the lysosomes. It could also produce toxins leading to symptoms of a disease or even death. In order for the organism to survive, it must be strong enough to fight off the disease by reproducing more cells.

The best current medical defense against viruses is the prevention of viral transmission. -AZT (Zidovudine) is an anti-retroviral medication (active against retroviruses like HIV that contain RNA as their genetic material). -When HIV injects its "insides" into the host cell (usually a CD4+ cell) it is injecting its genome (which is RNA) and reverse transcriptase enzyme -For HIV RNA to be able to infect our cells and turn them into factories, it first has to change its RNA into DNA so that it can integrate with our DNA. AZT is a Nucleoside Reverse Transcriptase Inhibitor and acts as a chain terminator and once it is incorporated, doesn't allow for further transcription. If HIV RNA cannot change fully into HIV DNA, it cannot permanently infect a cell.

Mutation of existing viruses Spreading out from an isolated population Transmission from one species to another

-A plant is infected from an external source of the virus. -become more susceptible to horizontal transmission of viral infections when damaged by wind, chilling, injury, or insects, all of which allow invading viruses to get past the plants' protective outer layer of cells.

-A plant inherits a viral infection from a parent -Can occur in asexual propagation or in sexual reproduction via infected seeds.

Naked RNA molecule which infects plants

Proteinaceous infectious particle that lacks nucleic acids and replicates by converting similar normal proteins into new prions. (mutation caused protein to have different folding properties)

- a prion is a misfolded form of a normal brain protein - when the prion gets into a cell with the normal form of the protein, the prion can convert the normal protein to the prion version, creating a chain reaction that increases their numbers

Eukaryotes: - made of linear DNA molecules, each contained in a chromosome -1 very long DNA molecule bearing thousands of genes associated with proteins that fold and pack the fine DNA into a more compact structure -# of chromosomes depends on species -paired chromosome -located in enclosed nuclear envelope -DNA packed with histones -lots of non-coding regions, introns present -large proportion of repetitive DNA -lots of genes -Genes are separated by long stretches of non-coding DNA -Individual genes transcribed seperately using Individual promoters Prokaryote: -has plasmid (singular) -single copy of chromosomes -located not enclosed in nuclear envelope -DNA not packed with histones -few non-coding regions, no introns -not a lot of repetitive DNA -few genes -Genes are closely packed, little non-coding DNA between genes -Genes in an Operon transcribed together using One Promote

Mitotic chromosomes Nucleosomes are the 11 nm beads on a string Folded into a 30-nm chromatin fiber 30-nm fibers form looped domains attached to protein scaffold Looped domains coil and fold Interphase Same up to looped domains Looped domains attached to inside surface of nuclear envelope

Nucleosomes = DNA wound around clusters of 8 histones with space in between Add histone H1, nucleosomes fold into a 30-nm chromatin fiber

More condensed, non-transcribed = heterochromatin Less condensed, transcribed = euchromatin

Tumor-suppressor genes make proteins that inhibit cell division Mutation might eliminate inhibitory activity Loss of DNA-repair ability Loss of ability to adhere Loss of cell cycle control

Normal function of Ras proto-oncogene Growth factor binds to tyrosine-kinase linked receptor Activates G protein, a G protein Activates a series of protein kinases Causes expression of cell cycle stimulating protein Mutation in ras May not need G protein stimulation; activates kinases on its own Ras may be hyperactive or more long-lasting

Activation of one (dominant) oncogene Inactivation of both alleles of (recessive) tumor-suppressor genes Activation of telomerase

Integrate their DNA into host cell chromosomes Causes mutation Can deliver or amplify oncogenes