Exam 2

chromosome

structure carrying genetic material

haploid cells

cells/organisms with unpaired chromosomes
1n,n

diploid cells

cells/organisms with paired chromosomes
2n

mitosis and cytokinesis

division of the nucleus
division of the cytoplasm and organells
2n cell- two 2n cells
daughter cell identical to parent cell

functions of mitosis

growth-sperm (haploid) and egg (haploid) (gametes)= diploid
repair/replacement- dividing bone marrow cells-> RBC
asexual reproduction

prior to mitosis

chromosome is replicated prior to mitosis
sister chromatids- replicated chromosomes
chromosomes become very compact at start of mitosis
centromere- region where sister chromatids attach at site of kinetochore formation

kinetochore

protein structure on chromosomes where microtubules attach during division to pull the chromosomes apart

binary fission

cell division in prokaryotes

control of the cell cycle

alternates between interphase and cell cycle
normal cells halt division at checkpoints
if conditions unfavorable -> process halted

Gap 1 (G1)

cell cycle
2n=4
signal telling them to divide
cell growth and transcription/translation occur

S phase

cell cycle
DNA replication
DNA synthesis

Gap 2 (G2)

preparing for mitosis
expressing genes needed for mitosis
centrosomes become visible, duplicate, microtuble organizing centers, microtubles grow from centrosomes

prophase

preparing to divide
chromosomes condense, nuclear envelope breaks down, centrosomes migrate to opposite poles of the cell, spindles form, MTS grow, some MTS attach to kinetochore (Microtuble kinetochore), polar MTS attach to poles

metaphase

chromosomes line up on metaphase plate

anaphase

seperation of sister chromatids, kinetochore microtubules will shorten, polar microtubles get longer and push against each other-> elongate cell

telophase

chromosomes de-condense, nuclear envelope reforms, mitotic spindle disapears

cytokinesis

microfilaments pinch cell in half

organelles divide

endomembrane system- fragmets into vesicle structures
reforms in daughter cells
mitochondria- split between two daughter cell, divide by binary fission to reproduce in new cell

cell cycle check points

G1 checkpoint, G2 checkpoint, metaphase checkpoint
G1 checkpoint- cell big enough, DNA in good shape
G2 checkpoint- is DNA replication complete
Metaphase checkpoint- are chromosomes attached to kinetochore MTS
if conditions are incorrect, cell cycle stopped- fix problem, move past checkpoint; can't fix problem, apoptosis; can't fix problem, cancer

how an external signals signal a cell to divide

reception-signal molecule binds to the the receptor
transduction-proteins in cell activated by receptor, phosphorylation cascade
response- activate cell cycle control proteins, turn on cell cycle control genes, activation of cell division

proto-oncogenes

genes that encode signals, receptors, signaling molecules, control proteins
mutated to oncogenes

how does a proto-oncogene become a oncogene

point mutation- mistakes in DNA replication, exposure to mutagens, virus inserting DNA into a gene
gene amplification- normal protein, but too many, too many gene copies, Ab can be made to bind to them and slow cell division

tumor surpressor cells

inhibit cell division, normal cell proteins
shut down cell division if conditions not favorable- detect and repair DNa damage, promote apoptosis, make sure cells are anchored
if mutated-cell cycle checkpoints ignored, damaged cells proliferate

p53

the master watchman
tumor surpressor protein
DNA damage and cell cycle abnormalities activate
leads to cell cycle arres, DNA repair, and cell cycle re-start or apoptosis
if mutated damaged DNA/cells go thru mitosis

human papilloma virus

integrates id DNA into host genome
host transcribe/translate hpv genes
creates E6 protein, which attaches ubiquitin to p53

epigenetic phenomenon

process that alters gene activity without changing the DNA sequence
leads to modifications that can be transmitted to daughter cells
modifications can be reversed
e.g. tumor surpressor genes silenced by aberrant methylation

telomerase and cancer

telomeres-ends of linear chromosomes, shorten with each cell division
telomerase(replicates telomere) activity is detected in almost all human tumors-> cell imortality

antisense RNA

inhibit telomerase
cancer treatment
single-stranded nucleic acid complementary to normal mRNA molecule mad by cell

chemotherapy

injection of chemicals into blood stream to kill dividing cells
some prevent cell division
some stop cell metabolism

radiation therapy

energy particles damage DNA-> cells destroyed/injured

asexual reproduction

offspring are clones
mitosis/cytokinesis
binary fission

sexual reproduction

two parents
gamete production (meiosis)
gamete meets gamete (fertilization)
offspring not indentical to parent

animal sexual life cycle

meiosis produces haploid gametes
fertilization (egg and sperm) produces diploid zygote
zygote divides, divides, divides by mitosis
meiosis-4 n daughter cells

sex chromosomes

xx-female
xy-male
other chromosomes are autosomes

human karyotype

2n=46
karyotype-chromosomes arranged in ordered pairs

meiosis cell cycle

G1- diploid cell in gonad 2n=4, cell growth
S- DNA replication, duplicated chromosomes
G2- cell growth, centrosomes double, appear
Meiosis- haploid gametes (do not go through cycle again)

prophase I

meiosis
chromosomes condense, nuclear envelope fragments, centrosomes migrate, meiotic spindle forms
alleles cross over

metaphase I

meiosis
homologous chromosomes align on metaphase plate
alignment on metaphase plate is random (independent assortment)
kinetochore MTS attached to kinetochores

anaphase I

meiosis
kinetochore MTs shorten
polar MTs lengthen-> cell elongates

telophase I/cytokinesis

meiosis
each half of cell has complete 1n set of replicated chromosomes
chromosomes decondense
nuclear envelope reforms
both cells enter meiosis II

prophase II

meiosis
meiotic spindle forms
chromosomes condense nuclear envelope fragments

metaphase II

meiosis
chromosomes aligned on metaphase plate

anaphase II

meiosis
sister chromatids seperated-> moved to opposite poles of cell

telophase II/ cytokinesis

meiosis
nuclei reform
chromosomes decondense

consequence of meiosis/sexual reproduction

seperation and distribution of homologous chromosomes produces genetic variation in offspring
random alignment of chromosome on metaphase plate
crossing over, each gamete is genetically unique
fertilization

nondisjunction

members of a pair of homologous chromosomes or a pair of sister chromatids fail to seperate properly from each other
nondisjunction at meiosis I and meiosis II

anueploidy

abnormal # of chromosomes
monosomy-lack of one chromosome n + (n-1), monosomy in autosome-always lethal, turner syndrome
trisomy-three copies of a chromosome n+(n+1), abnormal dose of genes on large chromosome, trisomy 21- down syndrome

fetal testing

blood test- 16-18 weeks
amniocentesis- 14-16 weeks, extract amniotic fluid
chorionic villus sampling- 8-10 week, part of placenta extracted

alterations in a chromosome structure

deletion-portion of chromosome deleted
duplication
inversion-segements all there butt turned around
reciprocal translocation-piece of one chromosome is moved to another chromosome

chromosome translocation

can cause a proto-oncogene to become an oncogene

blending hypothesis of inheritance

future offspring all have the same trait

particulate hypothesis

2nd generation crosses (F2 generation) crosses could give back traits from parents

phenotype

physical traits of an organism
phenotypic ratio- 3 purple flowers, 1 white flowers. 3:1
determined by genotype-genetic makeup of organism

allele

alternate version of gene
both the alleles can be the same (homozygous)
alleles can differ heterozygous
dominant allele- fully expressed in the organism's phenotype even if different allele is also present
recessive allele- has no noticeable effect on phenotype if dominant allele present
alleles seperate from each other during meiosis

testcross

use parent that only contributes recessive alleles to determine genotype of another parent

genetic predictions

based on probability
accuracy of predictions depend on sample size
probability that two or more independent events will occur is equal to the product of their individual probabilitis

huntington's disease

alleles dominant but uncommon
incurable, fatal neurological disease, median age of diagnosis is 38 years
trinucleotide repeat disease
near start of HTT gene, cag is repeated
too many repeats-> too many glutamines
# of CAG repeats correlated w/ severity of disease and age at onset

achondroplasia

mutation in fibroblast growth factor recepto gene
abnormality in cartilage/bone formation'
dwarfism

incomplete dominance

heterozygotes have intermediate phenotype
red and white flowers= pink

codominance

heterozygotes show both phenotypes
MN blood groups in humans
although a 2n individual can have only two alleles at any one locus, there may be multiple alleles in a population (ABO blood groups)

pedigrees

genetic traits in humans can be tracked through these

inheritance of sex-linked genes

sex of offspring determined by whats carried in the sperm (father determines sex of offspring)
males are heterozygous for sex-linked genes
many genes on the x chromosome
y chromosome genetic wasteland

inheritance patterns are complex

most genes have multiple phenotypic effects
genes interact
characters due to an additive effect of two or more genes
enviromental influence
epigenetic phenomena

x-inactivation

female inherits two x chromosomes
both are initially active but random inactivation occurs in one of the x chromosome, becomes are bar body
all x chromosomes inactivated in all daughter cells

energy and exchange

e- in chem bonds of food have lots of stored energy
we harvest the energy stored in the chem bonds of our food by cellular respiration
glycolysis occur in cytosol, krebs and e- transport in mitochondria

mitochondrial structure

outer mitochondrial membrane (omm)
inner mitochondrial membrane (imm) with cristae
cristae= huge surface area
intermembrane space
interior=matrix

glycolysis

sugar splitting, glucose-> 2 pyruvate
2 ATP (energy investment)
generate 4 ATP (net gain of 2 ATP)
2 NADH formed

pyruvate processing and krebs cycle

pyruvate moves into mitochondria and is converted Acetyl CoA (NADH produced) release CO2
krebs cycle- 3 NADH, FADH2, 2CO2, ATP (happens twice (once per pyruvate) for each glucose

substrate level phosphorylation

ATP made in glycolysis and krebs- enzyme grabs P from a molecule and transfers it to ADP

NADH and FADH2

e- shuttles
give up their e- to their e- to electron transport chain (ETC)
O2 is final e- acceptor

electron transport chain

NADH and FADH2 give up their e-
components can accept and donate e-s
complexes I, II, IV are also H+ pumps
e- move down ETC
e- connect with O2 and H to make water
e- provides energy for H+ pump (active transport)

ATP synthase

H+ flows through ATP synthase complex (facilitated diffusion) catalyzes formation of ATP
converts energy stored in H+ gradient to energy in form of ATP

oxidative phosphorylation

formation of ATP through combination of protein pumping by ETC and flow of protons through ATP synthase
for each NDAH 3 ATP
for each FADH2 2 ATP
34 ATP total

certain poisons interrupt critical events in cellular respiration

interfere with e- transport
disable ATP synthase
uncoupler-make inter mitochondrial membrane leaky so no proton gradient built up

fermentation

vs aerobic respiration
lactic acid fermentation
ethanol alcohol fermentation

protein, polysaccharides, fats in cellular respiration

a.a. used in pyruvate and acetyl CoA
glycerol from fats used in glycolysis with polysaccharides
fatty acids used in acetyl CoA

energy and exchange

property of life->homeostasis, internal condition in changing enviroment stays in steady state

animals exchange materials with enviroment

food, gases, wastes
simple animals-direct exchange, lots of surface area, little volume
complex animals have specialized exchange surfaces, exchange surfaces have large surface areas, connected to circulating system, and cells are bathed in interstitial fluid

four stages of food processing

ingestion
digestion
absorption
elimination

ingestion

the act of eating
bulk feeders-eat relatively large pieces of food, adaptions of tentacles, pincers, claws, poisons fangs. etc.
substrate feeder- animals that live in or on their food source
suspension feeder- sift small food particles from water
fluid feeders- suck nutrient-rich fluid from a living host

alimentary canal

digestion and absorption
different physical and chemical processes can be seperated
one way flow of food, allowing wastes to exit body at anus

digestion

food broken down into molecules small enough to absorb
mechanical-physical breakdown of food
mechanicl-physical breakdown of food, increase surface area for enzymes
chemical- enzymatic breakdown of food, polymers-> monomers

digestion in mouth

digestion starts here
mechanical and chemical digestion (saliva)
salivary amylase- starch/glycogen breakdown
lingual lipase- fat breakdown
mucins-lubricate food
antibacterial agents
bolus-travels via esophagus to stomach
peristalsis

digestion in stomach

function of stomach- storage, mechanical digestion (churning), and chem digestion (gastric juice)
gastric juice digests proteins
pepsin-protease (protein digesting enzyme)
hydrochloric acid- kills bacteria and unfolds proteins (pepsin has more surface area)

why gastric juice does not destroy cells that make it

epithelium of stomach forms deep pits, which contain specialized cells- mucus, parietal, chief
chief cells secrete inactive pepsinogen so it doesn't kill stomach lining, secreted when needed
parietal cells- secrete HCl activates pepsinogen, pepsin has positive feedback
mucus cells- secrete mucus
stomach epithelial cells- rapid mitosis

digestion in small intestine (SI)

chemical digestion continues with aid of accessory organs
acid chyme moves from stomach to SI, carbohydrates- pancreatic amylase, proteins-trypsin and chymotrypsin-proteases, secreted as inactive precursors from pancreas, lipids- bile made in liver, stored in gall bladder and pancreatic lipase, nucleic acids- nucleases made by pancreas

absorption

animal cells take up small food molecules for cellular respiration
occurs across small intestine, villi-folds, microvilli- folds on folds (large surface area)
many nutrients->bloodstream-> liver-> rest of body
fat->lacteals->lymph vessels-> bloodstream

elimination

undigested/unabsorbed food-> large intestine (LI)
functions of LI-absorption of water, excretion of solid waste, mutualistic relationship with prokaryotes

epithelial cells lining alimentary canal

connected with tight junctions- closely associated areas of two cells whose membranes join together forming a virtually impermeable barrier to fluid
hold cells together by proteins and inhibit movement of dissolved materials through the space between cells

evolutionary adaptions of vertebrate digestive systems

dentition- sharp teeth eat flesh (carnivore), flat teeth eat to grind and mash plant material (herbivore), omnivore has both
stomach-big meals, need expandable stomach
intestines- long SI for plant eaters- more time to digest and more surface area to absorb, larger cecum
ruminants- contain prokaryotes with cellulose-digesting enzymes, regugitation

respiration

exchanges gases
gases move across membrane by diffusion, move down pressure gradient
gases must be dissolved in water
gases move across respiratory surfaces

respiratory surface

variety of forms
common features- thin (few cell layers), large surface area, moist, composed of living cells, in contact with circulatory system- exception are insects

body surface (respiration)

lots of exposed surface area
exchanged directly thru cells
limitations- live in moist enviroment, have to be small, thin, flattened
most animals however- small body surface relative to volume or surface impermeable to gases

gills

highly folded extensions of body wall
adapted for gas exchange in aquatic enviroments
gas exchange is hard in water, much less O2, O2 diffuses much slower, flow over water is unidirectional, flow of blood thru gills is opposite direction of water (countercurrent flow)
aquatic organism will need larger respiratory surface
external gills- direct contact with water
internal gills- water driven over them, open close mouth and operculum to ventilate

counter current flow

flow of water is opposite of blood
O2 in H2O always higher than O2 in blood
gradient for diffusion all along capillary bed
co-current flow eventually becomes equilibrium

tracheal system

extensively branched system of tubules (insects)
adapted for gas exchange in terrestrial enviroments
contact with most body cells
contact w/ circulatory system not needed
ventilation of the tracheal system- small and inactive insects-> diffusion, large active insects-> muscle contraction

lungs

terrestrial vertebrates
infolding of the throat
respiratory surface is the alveoli of our lungs
trachea-lungs-bronchi-bronchioles-cluster of alveoli (huge surface area)
gases move by simple diffusion into bloodstream
move down pressure gradients- high O2 to low O2, high CO2 to low CO2

ventilation of lungs

breathing ventilates
negative pressure breathing-we pull air into lungs
inhalation- diaphragm contracts (moves down), pressure decreases and lungs volume increase and air flows in
exhalation- diaphragm relaxes (moves up), volume decreases and pressure increases (greater than enviroment)

our gas exchange not efficient

air flow is tidal-two way, depleted air and O2 rich air mix
residual volume- air left in alveoli after exhalation

ventilation of the bird lung

one-way air flow, air sacs
inhalation-air sacs fill
exhalation- air sacs empty; lungs filled
mostly one way air flow
parabronchi-respiratory surface
airflow is crosscurrent- air flows in one direction, gas exchange along entire respiratory surface

circulatory system

roles- deliver nutrients, deliver gases, remove wastes, circulate hormones, immune function
parts- circulating fluid, muscular pump (heart), set tubes

blood

composed of plasma and cells

red blood cells

transport oxygen, hemoglobin carries O2, cooperative binding- once one O2 binds 3 more bind quickly, binds reversibility

CO2 transported

some stays dissolved in plasma
some picked up by hemoglobin
most reacts with H2O in RBC and is then carried as bicarbonate in the plasma

three categories of vessels

arteris carry blood away from heart
veins return blood to the heart
capillaries convey blood between arteries and veins within each organ- capillary beds

structures of blood vessels fit their function

arteries- thick, muscular, elastic, withstand pressure of blood
capillaries- very thin, gases ,waste nutrients ,diffuse across
veins- skeletal muscle moves blood, have valves (blood moves one direction), valves go bad -> varicose veins

fish heart

two chambered heart
single circuit-blood goes thru two cap beds before going to heart, goes thru gill cap bed then systemic cap beds
blood pressure issues
slow delivery of O2 means less ATP made

amphibian heart

three chambered heart
double circulation- thru lung and skin caps then heart, then systemic caps
no blood pressure problems, but mixing of O2 rich and O2 poor blood

mammal and bird heart

four chambered heart
double circulation
provides vigorous flow of blood to tissues

endotherms

generates their own heat and maintain relatively constant body temp
evolution of a powerful four-chambered heart
have larger lungs, eat more, and put more energy into ridence of waste

ectotherms

body temp changes with enviromental temp.

waste disposal

undigested food-> feces
CO2-> respiratory surface
nitrogenous waste-> urine

nitrogenous waste

nitrogen- containing molecules breakdown
proteins-amino acids-amino groups- ammonia (toxic)-ammonium ion (increases pH of cell)

how animals get rid of toxic molecule

aquatic animals- ammonia or ammonium ions (high toxicity, low energy, high water loss)
mammals, amphibians, some marine fishes, some reptiles- urea (low toxicity, moderate energy, moderate water loss)
birds, insects, most reptiles- uric acid (low toxicity, high energy cost, low water loss)

kidney

produce urine
renal cortex, renal medulla, renal, pelvis, ureter
nephron-functional unit of the kidney, in medulla and cortex

the nephron

glomerulus- capillary enter nephron inside of bowmand capsule (blood filtering unit)
proximal tubule-close to bowman's capsule
loop of henle
distal tubule
collecting duct

urine formation-three main processes

filtration
reabsorption
final refining

filtration

extraction of water and small molecules from the blood, non-selective process (anything good or bad of the right size is filtered out of blood in the glomerulus)
filtered blood consists of large proteins, cells and platelets
filtrate enters proximal tubule

reabsorption

getting the good stuff from filtrate back into the bloodstream
reabsorption begins in proximal tubule (occurs throughout rest of nephron)
epithelial cells have microvilli-large surface area
H2O, salts, glucose, etc. enter epithelial cells then enter capillaries (aquaporins)
filtrate greatly reduced but more water still needs to be recoverd, loop of henle has many aquaporins- reabsorbs more water, medulla is hypertonic (facilitates H2O movement)

structure of nephron fits function

animals that do not need to conserve water-> freshwater fish- no loops of henle, aquatic mammals- short loops
desert animals- long loops of henle to conserve water

final refining

secretions-toxins, excess ions added to nephron
more water reabsorption
urine leaves collecting duct-> renal pelvis-> ureters-> bladder
regulation of refining- antidiruetic hormone (ADH)
neg feedback-change in a physiological variable triggers mechanisms that counteract change
ADH- triggered by high blood osmolerity in hypothalamus- causes thirst and reabsorption in collecting duct, triggers prodution of aquaporins

Exam 2

Zoology 101 with Bleiweiss\riters\thoma at University of Wisconsin - Madison

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