BIOL110: EXAM #3 UPDATED

photosynthesis

converts sunlight E to chemical E stored in sugar

equation for photosynthesis

light E + 6 CO₂ + 6 H₂O ——> C₆H₁₂O₆ + 6 O₂

location of photosynthesis

chloroplast (leaves major organs)

stroma

dense fluid surrounding thylakoid membrane

location of calvin cycle

thylakoid/thylakoid membrane

membranous sacs suspended within stroma; chlorophyll green pigments

location of light reactions

granum

sacks of sacs in thylakoid membrane

light reactions

converts light E to ATP and NADPH

splits H₂O into O₂

calvin cycle

uses ATP & NADPH to convert CO₂ to G3P (sugar)

returns ADP + P_i and NADP⁺ to light reactions

photosystem

reaction center complex + light-harvesting complex

reaction center complex

an organized association of proteins holding a special pair of chlorophyll a molecules and a primary electron acceptor

light-harvesting complex

various pigments molecules bound to proteins

photosystem II

functions first in light reactions…contains chlorophyll a P680

step #1 of LR

a photon of light hits the pigments in PSII

step #2 of LR

electrons being passed through from ground state to excited state and vice versa

step #3 of LR

excited electrons reach electrons of P680…electrons are transferred to the primary electron acceptor…in that process 2 electrons are lost to create P680⁺…PEA enzyme catalyzes H₂O into 2 H⁺ and ½ O₂

step #4 of LR

electrons reach PEA and are transported to the electron transport chain…electrons are passed from enzymes Pq to cytochrome complex to Pc and reach photosystem I

step #5 of LR

once the electrons reach cytochrome complex, ATP is created and H⁺ is pumped into thylakoid space

step #6 of LR

photons of light strikes photosystem I…photoexcited electrons that were transferred from PSII excited the electrons in PSI…electrons excited P700…P700 is then created into P700⁺ from the loss of electrons (redox reactions)

step #7 of LR

electrons reach the primary electron acceptor in PSI and are transported into the electron transport chain

step #8 of LR

electrons from the PEA are transported into enzyme Fd to NADP⁺…NADP⁺ and H⁺ are added to the enzyme and with the electrons from the PSI, NADPH is created

linear electron flow in light reactions

electrons flow throughout PSII and PSI…produces ATP, NADPH, and O₂ from net electron flow

carbon fixation

RuBP becomes unstable from the addition of CO₂…6 ATP are used to split RuBP into 3-PGA, which is also catalyzed by rubisco

reduction

the inorganic phosphate links onto the 3 PGA to create 1 3-biPGA…NADPH is split into NADP⁺ and P_i and creates 6 G3P (only 1 G3P output)

regeneration

5 G3P rearranged into 3 RuBP from the addition of 3 ATP…cycle continues

cell signaling

signal reception, signal transduction, cellular response

signal reception

target cell detects extracellular signaling molecule(s) via ligand/receptor binding

signal transduction

ligand binds to receptor…initiates transduction…ligand is relayed to elicit a specific cellular response

cellular response

transduce signals triggers the specific cellular response

ex: cytoskeleton rearrangement, gene activation

cell surface (transmembrane) receptor

binds to ligand outside of the cell…occurs in plasma membrane on target cell…ligand is known to be water soluble

intracellular receptor

binds to ligand either in the cytoplasm or nucleus that diffused through plasma membrane…ligand is known to be small, non-polar molecules or hormones

step #1 of GPCR

inactive receptor…G protein has GDP attached to it…enzyme is inactive

step #2 of GPCR

active…ligand binds to receptor via outside of cell…G protein binds to cytoplasmic side of the receptor…GTP replaces GDP

step #3 of GPCR

active G protein dissociates from receptor (ligand not present anymore)…G protein travels to enzyme and binds to cytoplasmic side of enzyme..enzyme activated and changes shape…initiates a cellular response

step #4 of GPCR

inactive again...G protein releases from enzyme and becomes GTPase…GTP turns into GDP plus an inorganic phosphate…available for use again once ligand is present

receptor tyrosine kinase (RTK)

catalyzes transfer of P group from ATP to tyrosine

step #1 of RTK

2 inactive monomer…ligand hasn’t bonded to ligand-binding site

step #2 of RTK

signaling molecules binds to ligand binding site…causes monomers to move towards each other and dimerize (bind)

step #3 of RTK

activated tyrosine kinase regions…6 ATP releases 6 inorganic phosphate…phosphates bind to tyrosine on receptor

step #4 of RTK

activated relay proteins bind to tyrosine-phosphate complex…initiates a 2 cellular responses…triggers transduction pathways

step #1 of signal transduction pathway

hormone diffuses across plasma membrane of target cell

step #2 of signal transduction pathway

hormone binds to receptor…activates hormone/receptor complex

step #3 of signal transduction pathway

H/R complex translocates to nucleus

step #4 of signal transduction pathway

H/R complex binds specific genes, functions as transcription factor

step #5 of signal transduction pathway

transcription activated + mRNA produced

step #6 of signaling transduction pathway

mRNA translocates to cytoplasm

step #7 of signaling transduction pathway

translocation activated…creates protein (cellular response)

second messenger cAMP

receives original signals and acts as a relay molecule

cAMP production

ATP…adenylyl cyclase removes two phosphate group…cAMP…phosphodiesterase converts cyclic AMP to AMP

omnis cellula e cellula

all cells come from pre-existing cells that have divided

binary fission

prokaryotic division (bacteria—>chromosomes replicated—>cell elognates—>2 separate cells)

G1 phase

metabolic activity and growth (making of proteins & organelles)

S phase

metabolic activity, growth, and DNA synthesis (DNA replication occurs)

G2 phase

metabolic activity, growth, and preparation for cell division

M phase

equal separation of DNA into daughter cells

G0 phase

non-dividing state

histones

pack DNA together during S phase

DNA replication

chromosome duplicates to become sister chromatids

centromere

links sister chromatids together

G2 of interphase

chromosomes duplicated, uncondensed

centrosomes with centriole pairs

prophase of mitosis

nucleolus disappears…mitotic spindle begins forming..chromatin condenses to chromosomes…centrosomes move away from each other

prometaphase of mitosis

nuclear envelope breaks down…spindle MTs attach to kinetochores and form kinetochore MTs

metaphase of mitosis

chromosomes align at metaphase plate…centrosomes are on opposite sides…equal tension

anaphase of mitosis

cohesion proteins cleaved…sister chromatids are pulled to opposite poles…cell elongates (MT lengthens)

telophase of mitosis

nucleolus reappears and nuclear envelope reform…chromosomes decondense…spindle MTs depolymerize

cytokinesis

division of the cytoplasm

cleavage of an animal cell

ring of actin filaments are pinch along cleavage furrow and make up two identical daughter cells

cell plate formation in a plant cell

cell plate formation occurs…different from cleavage furrow

G1 checkpoint

no DNA damage…sufficient resources (enough resources to divide)

S checkpoint

no replication errors

G2 checkpoint

no DNA damage after replication…chromosome set complete…enough cell components

M checkpoint

all sisters attached to mitotic spindle to both sides

apoptosis

cell death; cell fails checkpoints

growth factor

molecules that promote or inhibits mitosis affect differentiation

EGF

tells cell to divide (positive growth factor)…cell proliferation signal…cell survival

TGF

tells cell to stop and arrest (negative growth factor)…anti-proliferation signal…programmed cell death

cancer-critical genes

mutation contributes to causation of cancer; mutation in these genes lead to cancer

proto-oncogenes

positive growth factor…signals that cause a cell to divide

tumor supressor genes

negative growth factor…stops cell from dividing

oncogene

mutation in proto-oncogene…gain in function…signal doesn’t turn off

mutation in tumor supressor gene

loss of function…no more stop sign

cancer

complex, uncontrolled cell growth

proliferation

mutation in the genes that control the cell cycle

tumor formation

rapid multiplication of cells establishes a benign tumor, which can grow larger if it recruits a blood supply'; angiogenesis

invasion

tumor cells that start invading other tissues are cancer cells

taxol

a drug that inhibits the rapid cell growth of cancer by binding to the tubulin of microtubules

asexual reproduction

without fusion of gametes…1 parent produces offspring…genetically identical

sexual reproduction

fusion of gametes…2 parents give rise to offspring…genetic variation

karyotype

chromosome array by size & shape

somatic cell

all cells of body except gametes

gamete

sperm & oocyte

diploid

2 sets of chromosomes

human cell: 2(23) = 46 chromosomes

homologous chromosomes

length, staining, centromeres…inherited characters

autosomes

chromosomes 1-22

sex chromosomes

23rd pair…female: XX…male: XY

meiosis I

reduction division - all about the tetrads

prophase I

nuclear envelope breakdown…centrosome movement & spindle formation…chromosome condenses…crossing over occurs…tetrads form

tetrad

pair of duplicated homologous chromosomes; 4 chromatids

metaphase I

tetrads align at equator

anaphase I

homologs pulled to opposite poles

telophase I

daughters have homologous chromosomes…2 daughter cells