BIO 202 Midterm 3

structure of chlorophyll

the light absorbing region is the porphyrin ring with Mg atom (functions as co-factor). anchored to the thylakoid membrane by a hydrophobic tail.

chlorophyll A vs B

chlorophyll A has a CH3 group where chlorophyll B has a CHO group

photo-excitation of chlorophyll a

light makes an electron jump from the ground state to the excited state. the electron energy is transferred to the primary acceptor, which then leads to ATP and NADPH synthesis. the electron then falls back into the ground state (in an isolated system, energy from electron falling back into ground state is released as heat. in nature, the electrons are transferred to other molecules)

photo-excitation of chlorophyll b and carotenoids

only chlorophyll a can activate the primary acceptor. when chlorophyll b and carotenoids are excited by sunlight, they transfer energy to chlorophyll a once they fall back into the ground state. the chlorophyll a then transfers energy to the chlorophyll a in reaction center, then primary acceptor.

photosystem

pigments together with primary acceptor. pigments are divided into two categories- antenna (pigment molecules, chl a, chl b, carotenoids, gather light and transfer energy to reaction center) and reaction center (two molecules of chlorophyll a, close to primary acceptor, transfers energy to primary acceptor)

photosystem I (P700) and photosystem II (P680)

reaction center that has chlorophyll a that absorbs light at 700 nm, and reaction center that has chlorophyll a that absorbs light at 680 nm. they are associated with different proteins

how photosystems work

transfer electrons by cyclic electron flow (only in photosystem I, only ATP is made) or by non-cyclic electron flow (both P700 and P680, ATP and N ADPH are made). both are needed because while non-cyclic flow makes similar amounts of ATP and NADPH, the Calvin cycle uses more ATP then NADPH. additional ATP comes from cyclic flow

cyclic electron flow

electrons are transferred from photosystem I -> primary acceptor -> protein -> cytochrome complex -> protein -> photosystem I. produces energy for chemiosmotic synthesis of ATP

non-cyclic flow

step one - photosystem II absorbs light, electrons are activated and transferred to primary acceptor. the chlorophyll lost an electron
step two - an enzyme splits water into H+ and 1/2 O2. electrons are then transferred back to chlorophyll II. 1/2 O2 forms O2 and is released
step three - electrons from primary acceptor of photosystem II go through EC and release energy used to make ATP through photophosphorylation
step four - after ETC, the electrons go to photosystem I to reduce it (it has already been excited by light and lost an electron)
step 5: electrons go through second ETC to ferredoxin and NADP+ reductase to make NADPH for Calvin cycle

ATP synthesis in chloroplasts (photophosporylation)

driven by chemiosmosis (similar to oxidative phosphorylation in mitochondria). the ETC transfers H+ from the stroma into the thylakoid space, as the H+ flow back to the storm through ATP synthase, the energy of their movement is used to add inorganic phosphate to ADP to make ATP. the ETC is the cytochrome complex

ATP production in mitochondria vs. chloroplasts

mitochondria - oxidative phosphorylation, energy comes from food, protons are pumped from the matrix to the inter membrane space, ATP is made in matrix and utilizing NADH
chloroplasts - photophosphorylation, energy comes from sunlight, protons are pumped from stroma into the thylakoid space, ATP is made in the stroma and without utilizing NADPH

calvin cycle

ATP and NADPH are used to make sugar from CO2. no requirement for light. "fixes" CO2 into a simple sugar G3P or GAP (immediate product of Calvin cycle). G3P requires 1 CO2, 3 ATP, 2 NAHPH

reactions in Calvin cycle

carbon fixation - fixes carbon by attaching to receptor RuBP, catalyzed by enzyme RUBISCO. uses ATP
reduction - uses NADPH and ATP from light reactions to make 6 G3P. only 1 G3P exits the cycle
regeneration of RuBP - other 5 molecules of G3P are used to recreate RuBP. Calvin cycle is ready to start again.

different kinds of plants

C4 plants - spatial separation between CO2 fixation and Calvin cycle.
CAM plants - temporal separation between CO2 fixation and Calvin cycle.
C3 plants - no separation. this is most plants

C4 plants

corn, sugar cane. adaption to semi-dry conditions (stomata are open only partially during hot days). first, they fix CO2 into organic acids in mesophyll cells, then they transport these organic acids to another type of cells (bundle sheath), where the organic acids enter the Calvin cycle as carbon source. spatial separation between CO2 fixation and Calvin cycle.

CAM plants

cacti, pineapples. adaptation to dry conditions (stomata are closed during hot days). to prevent evaporation of water through stomata during the day, CO2 is only taken up at night and incorporated into organic acids. when there is light, organic acids enter Calvin cycle as carbon source. temporal separation between CO2 fixation and Calvin cycle.

structure of DNA

composed of nucleotides. phosphate group at the 5' end, OH at the 3' end, and a nitrogenous base. pyrimidines have a one-carbon ring (T and G), and purines have a two-carbon ring (G and A). nucleotides are linked by phosphodiester bonds between the OH and the phosphate

chargaff's rules

base composition varies between species.
number of A bases = T bases and number of C bases = G bases

semi-conservative DNA model

each daughter DNA molecule contains one old and one new strand

DNA polymerase

builds the new stand using the old strand as a template. catalyzes the addition of each dNTP (deoxynucleoside-triphosphate) from the 5' end to the 3' end.

primase

produces a complementary RNA molecule to start DNA replication called a primer, since DNA polymerase can only add to an already existing strand, the primer provides the 3' OH for DNA polymerase

DNA replication in prokaryotes

starts at special sites called origins of replication, where two DNA strands separate and open up a replication bubble. circular genome and single origin of replication. replication proceeds in both directions.

DNA replication in eukaryotes

proceeds from multiple origins of replication (~ 50,000 in humans) since chromosomes are linear and long. allow DNA to be replicated faster.

helicase

an enzyme that binds to each strand of the double helix and breaks that hydrogen bonds between the two strands

topoisomerase

relieves the strain on the double helix ahead of the replication fork

single-strand DNA binding proteins (SSBs)

prevent separated strands from joining together again by binding the separated strands and stabilizing

ligase

an enzyme that connects two fragments of DNA to make a single fragment

DNA polymerase I

removes the RNA primer from the 5' end and replaces it with DNA nucleotides added to the 3' end of the adjacent fragement

DNA polymerase III

synthesizes new DNA only in the 5' to 3' direction. uses parental DNA as a template, and adds nucleotides to an RNA primer or pre-existing DNA strand

leading and lagging strand

on the leading strand, DNA polymerase III moves in the same direction as the replication fork. on the lagging strand, DNA polymerase III works in the opposite direction of the replication fork (can only synthesize from 3' to 5'). therefore, the lagging strand is synthesized as a series of segments called Okazaki fragments, which are later joined together by DNA ligase.

accuracy in DNA replication

DNA polymerase III can proofread its work (checks the match between paired bases). if the enzyme finds a mismatch, it pauses and removes the mismatches base. unfixed error are a source of genetic variation.

the "end" problem during replication

after the last RNA primer is removed from the 5' end at the lagging strand, a shortened 5' end remains because DNA polymerase quires a 3'OH. the strand becomes shorter and shorter each replication. solved by telomeres

telomeres

a junk sequence with thousands of repeats of a single sequence. do not prevent by postpone the erosion of the ends of chromosomes. telomere shortening is associated with aging.

function of cell division

reproduction in single celled organisms, growth and development in multicellular organisms, and tissue renewal.

eukaryotic chromosomes structure

linear DNA molecule containing thousands of genes. negatively charged DNA is wrapped around positively charged histone proteins to form chromatin. a nucleosome is a basic unit of DNA packing, which is DNA wound twice around a histone octamer (8 units). The DNA is packaged in the nucleus. chromosome number varies across species

euchromatin vs heterochromatin

euchromatin are DNA regions that are more loosely packed and accessible for transcription. heterochromatin are DNA regions that are densely packed and generally not transcribed.

phases of the cell cycle

interphase:
in G1, the cell grows, copies its organelles, and prepares for the next steps
in S phase, the cell synthesizes a copy of the DNA in its nucleus. this results in two physically connected DNA molecules called sister chromatids held together by cohesin proteins
in G2, the cell undergoes a final period of rapid growth, and checks DNA for errors or damage
M phase:
in mitosis, the cell divides its genetic material and nucleus. chromosomes condense through condensin proteins
in cytokinesis, the cytoplasm of the cell is divided

centromere

a region made up of repetitive sequence sin the chromosomal DNA where sister chromatids are closely attached. the portion of a chromatid on either side of the centromere is called an arm. two arms per chromatid.

microtubules and MTOC

cytoskeletal polymers composed of tubular that can grow (polymerize) and shrink. centrosomes (two centrioles) are the major microtubule organizing center in cells. microtubules emerge from the centrosomes to set up the mitotic spindle.

centrosome dynamics during the cell cycle

the centrosome begins duplication during interphase in S phase. as mitosis starts, the two centrosomes are adjacent to the nuclear membrane. each centrosome nucleates microtubules and begins to form the mitotic spindle. as the microtubules grow in prophase, the centrosomes are pushed apart. by metaphase, the centrosomes are at opposite sides of the cell and the mitotic spindle is set up.

kinetochore microtubules

pull chromosomes to the poles of the cell during mitosis. the kinetochore is a protein complex that assembles on centromeres. microtubules from the spindle attach to chromosomes by binding the kinetochores. defects in attachment lead to unequal segregation of chromosomes.

prophase

chromosomes condense, the mitotic spindle begins to form, and centromeres are pushed towards opposite cell poles by the lengthening microtubules between them.

chromosome condensation in prophase

sister chromatids are held together by cohesion proteins before mitosis. during prophase, condensin II binds DNA and extrudes loops. the chromosomes become wider, shorter, and denser.

Prometaphase

the nuclear envelope breaks down and fragments. microtubules from the spindle begin to attach to the chromosomes via the kinetochores.

chromosome condensation in pro metaphase

with nuclear envelope breakdown, condensin I now has access to the DNA in the nucleus. condensin I forms new loops on the existing loops generated by condensin II, leading to further chromosome compaction.

metaphase

microtubules have captured all the kinetochores from opposite poles. pulling and pushing of kinetochore microtubules aligns chromosomes at the metaphase plate.

anaphase

each sister chromatid is operated from each other and pulled towards the pole it is attached to by the spindle fibers. after separation, each sister chromatin is considered a chromosome with equivalent genetic content.

chromosome separation during anaphase

the protein separase proteolytically cleaves cohesin, releasing the sister chromatids. separase activity is controlled by a large complex called the anaphase promoting complex

telophase

duplication groups of chromosomes have arrived at opposite ends of the cell. the nuclear membrane begins to reassemble, and chromatin becomes less tightly coiled.

cytokinesis

a contractile ring containing filamentous-actin (F-actin) and the moto protein myosin II constricts and separates the cell. a cleavage furrow forms.

G0

a resting stage of the cell cycle in which DNA replication and cell division stop. cells can re-enter G1.

what cell cycle control regulates

frequency and duration of cell cycle in different cell types.

premature passage through cell cycle causes

insufficient cell size, incomplete chromosomes replication ( loss of genetic material), or incomplete attachment of chromosomes to microtubules (daughter cell receives wrong number of chromosomes)

checkpoints in the cell cycle

points at which the cell stops unless it receives a go-ahead signal. once the cell goes through the checkpoint there is no going back (binary decision). the three major checkpoints at G1, G2, and M

G1 checkpoint

between G1 and S. cell decides to divide, delay division, or enter G0. this is a critical checkpoint, and when passed, commits the cell to completing the cell cycle. external signaling factors regulate cell passage through the checkpoint. factors bind to receptors on the target cell and cause an increase in cyclic production. the cyclin binds and activates Cdk. environmental factors include anchorage dependence (cells require a surface for division) and density dependent inhibition (when cells form a monolayer they stop dividing).

G2 checkpoint

checks if the cell is ready for mitosis, checks for DNA damage/completed replication. maturation-promoting factor (MPF) triggers the G2 -> M transition. MPF is the M-Cdk + M-cyclin complex. M-cyclin is produced in S-phase and destroyed in M-phase. MPF activity rises before M-phase and quickly decays at the end. MPF phosphorylates target proteins that trigger nuclear envelope, or condense chromosomes

M checkpoint (mitotic spindle checkpoint)

checks if all sister chromatids are attached to kinetochore spindles. the M-checkpoint is based on a signal to delay anaphase that originates at kinetochores not yet attached to spindle microtubules. defects in the spindle assembly checkpoint (SAC) can cause daughter cells to receive too few or too many chromosomes.

cyclins and cyclin-dependent kinases

cyclins are proteins that are produced in synchrony with the cell cycle (fluctuate in concentration with the cell cycle). cyclins have no enzymatic activity. Cdks are kinases that have no activity unless they are born to cyclins. Cdk protein levels are constant, while cyclins vary with the cell cycle. transfer a phosphate group to a target protein. cyclin binding causes a conformational change in a Cdk that allows it to be phosphorylated and fully activated. the active Cdk-cyclin complex can then go on to phosphorylate downstream targets to regulate the cell cycle

different kinds of cyclin and Cdks

G1/S-cyclin pairs up with G1/S-Cdk, S-cyclin pairs up with S-Cdk, and M-cyclin pairs up with M-Cdk.

Wee1 gene

Wee is a kinase that places an inhibitory phosphorylation on MPF. when wee is absent (mutated) M-Cdk is prematurely active. fission yeast will enter the cell cycle before growing to the correct length, meaning that it will be shorter.

Cdc25 gene

a phosphatase that removes the inhibitory phosphate placed by Wee1. when absent (mutated), M-Cdk + cyclin stays off. the fission yeast will sit in G2 and continue to grow.

cancer

a growth disorder of cells. arise when single cells are unable to follow growth rules and proliferate uncontrollable, usually at the expense of neighbors. have two heritable properties: reproduce in uncontrolled manner, and invade and colonize other cells. cells that only reproduce in an uncontrolled manner form a benign tumor, while cancer cells that do both are malignant. accumulated mutations lead to cancer.

two genes that can cause cancer

proto-oncogenes and tumor suppressors

proto-oncogenes

genes that cause normal cells to be cancerous when mutated. stimulate cell growth and division, and stop cell death. this is a gain-of-function mutation, meaning that a mutation in one gene (out of two) is enough to cause cancer. mutated proto-oncogenes become oncogenes.

tumor suppressors

regulate the cell cycle, stopping it at various points. mutations cause a loss of function. phenotype manifests when both copies of the gene are inactivated.

haploid and diploid gametes

haploid gametes carry a single set of chromosomes (n). diploid gametes carry two sets of chromosomes (2n).

sexual life cycle

fertilization and meiosis alternate. in humans, fusion of egg and sperm produces the diploid zygote. the zygote produces somatic cells by mitosis that develop into an adult. organisms such as yeast spend most of their life cycle in the haploid state, and unlike humans, these haploid cells can go through mitosis.

somatic cells vs germ cells

somatic cells form the body of the organism and go through mitosis. germ cells transmit genetic information for parent to offspring (meiosis). the germline can be considered an immortal lineage that is passed down indefinitely.

human chromosomes

humans have 46 chromosomes. males have 22 pairs, females have 23 pairs. 2 sex chromosomes, 44 autosomes.

meiosis

composed of meiosis I and meiosis II. in meiosis I, homologous chromosomes pair and then separate. this reduces the chromosomes number per cell by half. crossing over also occurs in meiosis II, sister chromatids are separated, resulting in four daughter cells with half as many chromosomes as the parent.

prophase I

takes 90 percent of the time in meiosis. the nuclear envelope begins to break down and chromosomes condense, and the mitotic spindle is forming. this is when the homologous chromosomes pair (synapse). crossing over occurs, forming bridges (chiasmata) that physically hold homologous chromosomes together. DNA is exchanged between non-sister chromatids.

synapsis in prophase I

homologous chromosomes physically connect. the DNA breaks occur at equivalent locations on non-sister chromatids, to facilitate crossing over. homologous chromosomes are glued together by the synaptonemal complex, across their entire length (facilitated by having the kinetochores act as one complex, differently from mitosis) sister chromatids are still held together by cohesins.

crossovers during prophase I

DNA breaks are repaired by joining DNA on one non-sister chromatids to the corresponding segment of DNA of the other non-sister chromatid (this is a crossover)

metaphase I

pairs of homologous chromosomes are captured by kinetochore microtubules and arranged at the metaphase plate. the kinetochores act as one.

anaphase I

cohesion's linking sister chromatids are cleaved by separase everywhere except at the centrosomes. cohesin cleavage leads to the separation of homologous chromosomes. sister chromatids remain together because the cohesin remains at the centromeres and their kinetochores are linked

telophase I and cytokinesis

separated homologous chromosomes form a cluster at each cell pole and the nuclear membrane reforms around each daughter nuclei. daughter cells have half the number of chromosomes as the parents cell. each chromosome contains two sister chromatids (which are non-identical due to crossing over)

meiosis II

no DNA replication occurs before. same mechanism as mitosis.

events unique to meiosis

all occur during meiosis I. synapsis and crossing over in prophase I, pair homologous chromosomes lining up in metaphase I, and homologous chromosomes separate and are pulled to opposite poles.

origins of genetic variation

independent assortment of chromosomes, crossing over, and random fertilization

independent assortment

each pair of homologous chromosomes can be arranged in one of two ways independently of other pairs. genes are sorted independently of each other. number of different gametes that can form is 2^n, where n = haploid number

random fertilization

a human egg representing millions of possible chromosome combinations is fertilized by a single sperm that also representing millions of possible chromosome combinations.

true-breeding lines

plants whose offspring resemble parents over many generations, obtained by self pollination

homozygous and heterozygous

homozygous is 2 copies of same allele, heterozygous two different alleles

alleles

different versions of a genes. can be dominant or recessive.

Mendel's law of segregation

two alleles segregate independently during gamete formation and unite during fertilization.

Mendel's law of independent assortment

two genes or more assort independently.

probability rules

for independent events, the probability they both happen is the probability of A x the probability of B.
the probability that one of any two or more mutually exclusive events (one or the other) can be calculated by adding their individual probabilities.

complete, incomplete, and co-dominance

complete dominance is when the phenotype of the dominant homozygote and the heterozygote are indistinguishable
incomplete dominance is when neither allele is completely dominant.
co- dominance is when two dominant alleles affect the phenotype in separate distinguishable ways

incomplete dominance

example is that red and white flowers make pink flowers. the mechanism underlying this is that one allele does not produce enough pigment to create a red flower, therefore the flowers are pink. this is a case where the allele codes for enzymes that synthesize the red pigment. usually 1:2:1 ratios, with the 2 being the blended trait

co-dominance

example is in MN blood group gene, which has two co-dominant alleles that regulate the production of different surface molecules. when heterozygous, both types of surface molecules will be produced.

human ABO blood type

three alleles are IA, IB, and i. IA and IB are co-dominant, while i is recessive. IAIA or IAi results in an A phenotype, IBIB or IBi results in a B phenotype, and IAIB results in an AB phenotype, and ii results in an O phenotype.

pleiotropy

a single gene affects more than one phenotype. example is sickle cell disease (caused by a recessive allele for a gene that produces hemoglobin)

epistasis

the expression of a gene at one locus alters the phenotypic expression of a gene at a different locus. example is in dog fur color. one gene determines pigment color: B for black, b for brown. a second gene determines whether the pigment will be deposited in hair: E for color, e for no color. phenotypic ratio will be 9:3:4

polygenic inheritance

multiple genes independently affect one trait. quantitative variation of a feature across a population usually indicated polygenic inheritance. example is skin color, with multiple genes contributing.

environmental impact on phenotype

some phenotypes are dependent on environment, like how nutrition influences height. some mutations may be temperature sensitive.

chromosomal abnormalities that alter mendelian inheritance

nondisjunction- homologous chromosomes or sister chromatids fail to separate. can occur during meiosis or mitosis.
duplication- extra copies of a chromosomes region. usually coupled with deletion.
deletion- missing chromosome regions. can occur during crossing over in meiosis prophase I.

causes of nondisjunction

defects in kinetochore microtubule attachment to chromosomes, inactive spindle assembly checkpoint, or defects in cohesin or separase.

nondisjunction errors in meiosis I

homologous chromosomes fail to separate (occurs in the parent cell). other sets of homologous chromosomes separate properly. all four gametes from this parent cell will have an abnormal number of chromosomes, either more or less (called aneuploidy)

nondisjunction errors during meiosis II

when sister chromatids fail to separate, usually only happens in one of the two daughter cells after meiosis I. the two granddaughter cells from the affected daughter cell with have an abnormal number of chromosomes. results in different (n+1) gamete than nondisjunction in meiosis I.

result of fertilization of gametes with nondisjunction errors

results in offspring with abnormal chromosome numbers. the offspring will have one of two conditions:
trisomy- cells have one extra copy of a chromosome (2n+1)
monosomy- cells have one less chromosome (2n-1)