AP Bio - DNA strucfunc, Replication, Telomeres, Mutations, Cell Cycle and Mitosis (Unit 8??)

Apoptosis is ______ cell death where _____ and ____ are specifically activated to chop up the ___ and then ___.

programmed, nucleases, proteases, DNA, organelles

Necrosis is _____ death of cells that occurs when the cells doesn't have access to ______.

premature, blood supply

Why do cells divide?

To grow, repair (wounds/injuries), replace, to reproduce (in bacteria), development

What is unique about chromatin form? (compare to chromosomes, talk about the specific protein involved, why it is the way it is, what phases of the cell cycle its involved in)

Chromatin is more loosely compact than chromosomes but is still wrapped very tightly around histone proteins (helix molecule wrapped around histone proteins to form "beads on a string" structure, each "bead" being a nucleosome) to organize it and allow it to fit in the nucleus. It is loosely coiled enough so that enzymes can get into the DNA to copy it -> make mRNA for protein synthesis. It is the normal form of DNA during all phases of the cell cycle except mitosis (basically only interphase).

What is unique about chromosome form? (compare to chromatin, why it is the way it is, what phases of the cell cycle its involved in, and how it is protected without a nucleus)

Chromosomes are compacted much more than chromatin, which means that their DNA cannot be read or copied in this form as it is so tightly wound. It's formed solely in mitosis in order to divide the doubled DNA from S phase in half through telekinesis. DNA is protected from destructive enzymes in this form because they can't get into such a tight structure needed without a nucleus to protect chromosomes.

One key difference between animal cell and plant cell telophase is that plant cells do not have _____ in their _____ but animal cells do.

centrioles, centrosomes

Why can't plant cells pinch apart like animal cells and form cleavage furrow?Ｗhat do they do instead?

In the middle of the cell vesicles line up to form the new cell wall which will separate the plant cell into two. They can't pinch because of the already existing cell wall.

chromatid

half of a chromosome

sister chromatid

each half of the same chromosome

centromere

complex of proteins attached to DNA holding the sister chromatids together

kinetochore

complex of proteins to the outside surface of the chromosome at the centromeric region where spindle fibers attach

What happens in G1?

When the cell is carrying out its "normal functions" mainly synthesizing proteins and is the phase the cell spends the most time in

What happens in S phase?

DNA is synthesized through replication

What happens in G2?

Mainly produces the proteins and enzymes necessary for mitosis (not made in G1 because there's no point in making mitosis proteins which will be inactive for so long) however no actual growth of the cell occurs

Explain how checkpoints work (like in between G1 and S) and how the cell transitions to different phases of interphase.

They are signaled to progress from one phase to the next by cyclin-dependent kinases to phosphorylate the enzymes of the next step, and checkpoints are signaled by inhibiting the kinases. Of course, when moving onto the next step, it also deactivates the enzymes that were just at work beforehand, so for example from G1 to S the cell inactivates translation enzymes and activates replication enzymes.

What happens in G0?

G0 does basically the same thing as G1 except that a cell in G0 is likely to stay in that phase and will not divide (not continue with cell cycle)

Why do many cancer cells have a mutation in the p53 gene? What does it regulate and what is the result of the mutation that leads to development of cancer?

The p53 gene, among many other functions, controls turning on apoptosis, so when the gene is messed up the cells can't undergo apoptosis even when the checkpoint recognizes abnormalities. This leads to unregulated cell division and cancer. In cancer, sometimes it's not that the cells themselves are dividing faster, it's just that the rate of cell division (which is normal) overpowers the rate of cell death because apoptosis isn't being initiated.

Why is apoptosis considered to be a part of the cell cycle?

We are constantly renewing our cells and to maintain proper size and functionality of our organs and tissues, there must be a rate of cell death that matches rate of cell division.

In the cell cycle, when is the DNA ONLY in chromatin form?

Interphase

In the cell cycle, when is the DNA ONLY in chromosome form?

Metaphase and Anaphase

In the cell cycle, when is the DNA in BOTH chromosome and chromatin form?

Prophase and telophase

In prophase, _______ begins to condense into ______ and become visible in the _____. The ______ ____ begins to break down, and centrosomes ____, form ____, and move to the ____. Proteins attach to _____ forming ____ and spindle fibers attach to ____, so the ___ begin moving.

chromatin, chromosomes, nucleus, nuclear membrane, duplicate, spindles, poles, chromosomes/centromeres, kinetochores, kinetochores, chromosomes

In metaphase, _____ are lined up in the equator by the ___. In anaphase, the sister chromatids separate at the _____, and each chromatid (which is now a ______) heads to the ___ of the cell. The movement is due to ______ movement along the _ _ _.

chromosomes, spindles, centromeres, chromosome, poles, kinetochores, spindle fiber microtubules.

In telophase, ____ separate completely to the opposite ____. New ___ start to form around the _____, and the ____ begin to ____ back into ___. ___ begins to pinch in animal cells and a cell wall begins to form in plant cells, which is called _____.

chromosomes, poles, membrane, DNA, chromosomes, decondense, chromatin, cytoplasm, cytokinesis

What happens after telophase and cytokinesis have complete? (also describe the state of the 2 new cells)

The cells reenter interphase and go about their normal business (synthesizing proteins as a tissue, replication of DNA for division again, preparing enzymes and proteins necessary for mitosis). The DNA is completely decondensed, new nuclei are reformed, and 2 totally new functioning cells exist.

Let's say that we have a cell with 20 chromosomes. Fill out the chart to keep track of amount and type (single/double) of chromosomes through the cell cycle.

G1:

G2:

Anaphase:

Daughter cells:

20 single (actually in chromatin in this state but just thinking of it in terms of chromosome for comparison)

20 double (actually in chromatin in this state but just thinking of it in terms of chromosome for comparison) (simply doubling each chromosome instead of changing chromosome number in S phase)

40 single (separation of sister chromatids doubles chromosome number)

20 single (actually in chromatin in this state but just thinking of it in terms of chromosome for comparison)

Example of cyclins amount being overriden by checkpoint factors

As the G1/S transition, the cell is checking: _____________________________________

Let's say there is DNA damage. This activates the p53 gene. The p53 protein causes production of ____ ___ and blocks the ___ ___ protein - the cell will stay in ____ until repair is made.

size, nutrients, growth factors, DNA damage

cdk inhibitor, cdk-cyclin, G1

How else do proteins inhibit the cell cycle to be halted if something is wrong? (not apoptosis or g0)

Cyclins/kinases (so either build up of the cyclins or kinases themselves)

Cdk complexes

Growth factors and attachment proteins can also impact the cyclins and kinases to speed up or slow down the transition (external factors)

DNA gives the information that specifies what ______ to make and therfore governs the function of the ___. DNA passes a copy of the info to ____ ____ through ___.

proteins, cell, new cells, replication

Similar to how macromolecules are just larger molecules made up of smaller molecules, proteins are ______ made up of many ____ ____ bonded together, and a DNA molecule is a _____ made up of many ____ bonded together.

polymers, amino acids, polymer, nucleotides

Purines (which of the 4 bases are they, bigger or smaller nitrogenous bases and how many rings of the bases)

Adenine and guanine, larger, 2 rings

Pyrimidines (which of the 4 bases are they, bigger or smaller nitrogenous bases and how many rings of the bases)

Cytosine and thymine, smaller, 1 ring

Chargaff's rules stated that DNA from any species of any organism should have a ___ ratio of _____ and ____ bases. (i.e. _+_=_+_). The amount of guanine should be equal to the amount of _____ and the amount of adenine should be equal to the amount of _____. His experiment showed ____ ___ ____ in ____, as A matches up with _ and C matches up with _.

1:1, purine/pyrimidine, A, G, T, C, cytosine, thymine, specific base pairing, nucleotides, T, G

The inner portion of the DNA molecule are the ___ ____ and the outer portions have the ___ ____ ____. The bonds holding the inner portion together are _______ bonds (so the strands are easily _____ and _____) while the bonds holding the outer portion together are ______ (so the ______ ___ can stay in order).

nitrogenous bases/purine-pyrimidine pairs, sugar phosphate backbone, hydrogen, separated/replicated, covalent, nitrogenous bases

Why do purines ONLY bond with pyrimidines? Why does only A pair with T and G pair with C?

To ensure base pairs are the same length in the middle (would either be too short or too long with purine-purine or pyrimidine-pyrimidine pairs) to keep the sugar phosphate backbone straight so its covalent bonds aren't strained. A+T and G+C is the only way to ensure exact copying due to its H bonds

Described what happened and what was discovered in Fred Griffith's experiment.

Injected mice with rough/nonvirulent -> mice lived

Injected mice with smooth/virulent -> mice died

heated up virulent bacteria -> bacteria was killed -> mice lived

Mixed non-virulent/rough strain and the heated smooth virulent strain -> mice died (unexpected)

The characteristic of virulence was passed on from the dead bacteria to the live bacteria through bacterial transformation.

How did Avery, Macleod, and McCarty piggyback off of Griffith's experiment?

This group took the new strain of bacteria from the dead mice in Fred's last treatment and used enzymes to break apart proteins, RNA, etc. When they broke apart DNA, this destroyed the extract's transforming power, and virulence was not passed onto the nonvirulent bacterial, which proved the DNA was the hereditary factor.

What did Hershey and Chase do to confirm whether hereditary material was proteins or DNA?

They used bacteriophages and radioactively labeled protein and DNA sections of the phage, and radioactivity had been found in the DNA parts which means that DNA and not protein had entered the cells.

Watson and Crick proposed that replication was...

semi-conservative (each of the two resulting DNA molecules contains an original and a new synthesized strand)

How did scientists disprove that DNA replicated conservatively or dispersively?

Once the DNA replicated once in the tube, only one band showed, ruling out conservative model (1 pure original 1 pure new). They replicated it a second time and saw 2 bands, which meant DNA replicated semiconservatively as dispersive would still only have 1 band. (used radioactive isotopes to measure and see this)

How does replication overcome random base pairing and tangling? How do you copy so many base pairs in mere hours? How do you make sure that you don't miss anything?

DNA is wrapped around histones and only open up little by little (by helicase) with proteins to prevent tangling. Base pairs are copied very quickly because replication has multiple origins, with several DNA polymerases working at once. We make sure we don't miss anything as DNA is only added on the 3' end (unidirectional)

How do we recognize 3' and 5' ends in a molecular representation of a DNA molecule?

5' end has a hanging phosphate group while the 3' end has a free OH group.

DNA builds to _' to _' (_____ strand) while it copies/replicates from _' to _' (____ strand).

5, 3, leading, 3, 5, lagging

At the start of replication, ____ is opened at the ______ of replication. ______ _____ binding proteins help hold it open temporarily, and _____ unzips DNA. _____ primase adds ____ primers - _ on leading strand and ___ on lagging strand.

DNA, origins, single stranded, helicase, RNA, RNA, 1, many

In the second step, after DNA has been opened, ___ polymerase ____ adds the complementary ______ on the ____ strand until it hits the next ____ of replication.

DNA, III, nucleotides, leading, origin

DNA ______ can only add onto the _' end of the growing strand. For the lagging strand, DNA ______ ____ add complementary _____ on it forming _____ _____.

polymerase, 3, polymerase III, nucleotides, Okazaki fragments

After Okazaki fragments are formed, ____ _____ are removed and replaced by ___ _______ _. ___ _____ fuses with the Okazaki fragments and any pieces not bonded together yet, and DNA _____ ____ (or DNA ______ _) check for mistakes, which happens as ___ __ are added.

RNA primers, DNA polymerase I, DNA ligase, proofreading enzymes, polymerase II, base pairs

Telomeres are repetitive ___ _____ at the ends of each piece of _____ that are _____. They are necessary to stabilize the ____ so they don't stick together/break. The ends of the ___ can't be ___ and they ____ with each replication, and only the ____ are shortening. _______ is and enzyme that adds the ____ back on and is only produced ________ and in ____.

DNA sequences, chromatin, obsolete, chromosomes, DNA, copied, shorten, telomeres, telomerase, telomeres, embryonically, cancer

Why/how exactly are the telomeres shortening?

DNA polymerase III needs a 3' end to add more nucleotides to fill up gaps after RNA primer is removed. It does this normally for every piece of the DNA except the very end of the molecule where there is no 3' end, and so a gap remains there. After several replications, DNA telomere region gets progressively shorter and shorter.

Why are cancer cells "immortal?"

Since cancer cells have turned back on the telomerase gene, they are dividing faster than normal (think back to cell cycle and not apoptosing) they should eventually stop dividing but they don't because telomeres aren't shortening from generation to generation.

Point mutations

Substitution - one base exchanged for another

Frameshift mutations

Insertion - a base or bases are added

Deletion - a base or bases are lost

How can mutations occur?

Mistakes in replication not picked up by neither DNA polymerase nor proofreading enzymes

Environmental insults (radiation, toxic chemicals in air, food, smoke)

Heat, even body heat

What are some ways how mutations can not change anything in the cell at all?

Repair enzymes might fix them (different from proofreading enzymes)

Cell undergoes apoptosis before entering S phase

Mutation might be in a gene that isn't read

May code for the same protein

What are some ways how mutations CAN change something in the cell?

The cell can make a misshapen protein, which may or may not cause the cell to malfunction, and if it does it could die or become cancerous

Unless the cell becomes ____, the malfunctioning cell WILL NOT change or affect the organism as a whole. In order for a mutation to have an effect on the organism as a whole, it MUST occur in the ____, ___, or ______. This will cause every cell of the offspring's body to have the mutation and change the trait of the organism.

cancerous, sperm egg and embryo