Biology Flashcards
microfilaments
- ACTIN (use myosin + ATP for movement)
- also in cytokinesis to contract cell
microtubules
- hollow polymers of tubulin
- uses kinesin + dynein to carry vesicles in cell
- cilia/flagella = in eukaryotic motile cells
- centrioles = in centrosome, organizing centre for microtubules
intermediate filaments
- cell-cell adhesion, integrity, resist tension, anchor
- ketatin, lamin, desmin, etc.
archaea
- single cells, look like bacteria but eukaryotic function
- circular chromosome, binary dfission
- eukaryotic: wrap DNA with actual histones, begin with Met, RNA polymerase same
types of bacteria metabolism
obligate aerobes
obligate anaerobes
facultative anaerobes
aerotolerant aerobes
3 types of bacterial genetic recombination
transformation = integrate foreign DNA with plasmids
conjugation = mating (donor, female)
transduction = need VECTOR, virus transports DNA/RNA
positive sense VS negative sense viral genome
positive sense = ssRNA directly translated
negative sense = ssRNA make complementary strand first (RNA replicase)
viral life cycle:
- infection
- translation/assembly
- progeny release
lytic (virulent) VS lysogenic (dormant, integrate provirus into genome)
prions
nonliving infectious proteins
convert alpha helix > beta sheet, protein aggregates
viroids
small pathogens living in plants, bind RNAs + silence genes
cell cycle overview
- G1 = least amount of DNA, increase size, grow organelles
- G1/S checkpoint = make sure DNA good to replicate p53
- S = replicate DNA ploidy doesn’t change, 2n»2n
- G2 = more growth
- G2/M checkpoint = ensure all organelles, cytoplasm, correct DNA replication
mitosis vs meiosis
- 2n>2n VS 2n>n
- meiosis I similar to mitosis, but meiosis II very different
- crossing over in meiosis
- homologous chromosomes pair in meiosis
nondisjuction in meiosis I
causes two n-1 cells and two n+1 cells
all 4 gametes abnormal ploidy
nondisjunction in meiosis II
only 2 gametes affected, 2 normal
one n-1, one n+1
order of sperm flow
SEVE(N) UP
oogenesis
- each oogenia = ONE functional oocyte
- primary oocytes born with 2n, arrested in prophase I (meiosis)
- during ovulation, meiosis I –> secondary oocyte (n) –> fertilization –> meiosis II
2 layers of oocyte
zona pelucida = surrounding oocyte, proteins + compounds
corona radiata = surrounding cells, attached to oocyte
male sexual development
- androgens during fetal period causes male sexual differentiation
- testosterone = develops reprod. system and secondary sex characteristics
- FSH stimulates sperm maturation
- LH causes testosterone production
female sexual development
- estrogen secreted due to FSH, secondary sex charaxcteristics
- estrogen regenerates uterine lining, but progesterone (secreted by corpus luteum) maintains it
menstrual cycle:
- follicular phase = GnRH releases LH/FSH, develops follicles, estrogen thickens lining
2. ovulation = LH PEAK - luteal phase = released follicle forms corpus luteum, secretes PROgesterone to develop lining – high est/progest = low LH/FSH
- menstruation = high progesterone buildup causes low LH, uterine layer shed, corpus luteum no longer to secrete est/progest, so causes GnRH to be stimualted again (low LH = corpus luteum lost)
- pregnancy = blastocyst releases hCG (analog of LH) that maintains corpus luteum
cortical reaction
after sperm penetrates egg, relese of Ca+ ions
depolarizes egg membrane to prevent another sperm, increases metabolic rate
blastocyst
ICM (becomes organism) and trophoblast (placenta)
gastrulation: 3 primary germ layers
- ectoderm = NS, hair, skin, nails
- mesoderm = support structures, muscle, bone, excretory, circulatory, gonads
- endoderm = epithelial linings, pacreas, thyroid, bladder
fetal circulation
- fetal arteries = DEOX blood from fetus to placenta
- fetal veins = OX blood from placenta to fetus
- gas exchange occurs at the placenta
- don’t want baby’s blood and mothers to mix
- detoxification by mother’s liver, nutrient/waste exchange at placenta
- 3 shunts
fetus: 3 shunts to direct blood away from its organs
- foramen ovale RA-LA = blood skips Right ventricle to bypass lungs, directly into body
- ductus arteriosus = shunts blood in pulmonary artery to aorta
- ductus venosus = shunts blood from placenta (umbillical vein) to inferior vena cava (bypass liver)
3 trimesters: overview
- heartbeag 22 days, 8 weeks = fetus, organ systems made
- growth, moves
- growth, LESS movement, antibodies transferred
specific neuroglia
- support / defense / immune system
- astrocytes = BBB
- microglia = break down waste products
- oligodendrocytes (CNS) and schwann cells (PNS)
action potential notes
- resting potential = -70mV (inside)
- cells = salty bananas
- Na+/K+ ATPase = “pumpKin” to restore balance
- axon hillock = threshold, trigger zone, voltage gated Na+ channels open
- hyperpolarization = refractory period prevents another signal
- local anesthetics block Na+ channels preventing pain impulses
- end of axon, Na+ channels open, Ca+ rushes in, NT vesicles released, enter synapse
reflex arc
- only processing at spinal cord level
peptide hormones
- bind EXTRACELLULAR, trigger cAMP signalling cascade
- end in “in” “ine”
- rapid but short-lived
steroid hormones
- bind INTRACELLULAR receptors
- cholesterol-based, cross membrane
- “one” “oid”
- slower but long-lived
AA hormones
- unpredictable
- catecholamines = fast lived, short lived (peptide-like)
- T3/T4 = slow onset, long lived (like steroid)
tropic hormones
stimulate production of another hormone by another gland that acts on a tissue, eg. ACTH
pituitary gland
- anterior = vascular connection (HTHPP): GH, TSH, FSH, LH, ACTH, PRL
- posterior = neural connection (tract): store + release oxytocin + ADH from hypothal.
thyroid
- controlled by TSH, T3/T4 = metabolism
- calcitonin = tones down Ca+
- PTH = increases Ca+
3 types of corticosteroids in adrenal cortex (sugar, salt, sex)
- glucocorticoids = cortisol (raise blood sugar)
- mineralocorticoids = aldosterone (increase Na+/H2o reabsorption to increase BV and BP)
- corticak sex hormones = androgens/estrogen
aldosterone pathway
- low BP sensed by juxtaglomerular cells
- cells secrete RENIN – celaves angiotensin to angiotensin I
- ACE converts angiotensin I to angiotensin II
- angiotensin II stmulates adrenal cortex to release aldosterone to increase BP
adrenal medulla
- ectoderm, NS, fast acting, not essential for life
- catecholamines (E, NE) – sympathetic fight/flight
pancrease cells
alpha = glucacon
beta = insulin (destroyed in type I, low receptor sensitivity in type II)
delta = somatostatin (inhib. both insulin + glucagon), reelesed by high BG/AA’s
pineal gland
secretes melatonin
circadian rhythms
EPO
released by kidneys
production of RBC’s
ANP
released by the heart
regulates salt/water balance
promotes excretion, deceases BV and BP
types of steroid hormones: list
- cortical hormones (all)
- testosterone, estrogen, progesterone
types of AA hormones: list
- T3/T4
- any other hormone is a PEPTIDE hormone
diaphragm is under ____ control
somatic control
but breathing is autonomic
surfactant
on alveoli
REDUCES surface tension
prevents collpase of alveoli during exhalation
negative pressure breathing
diaphragm contract, pulls downwards, increase V, decrease P, air sucked in from low pressure
total lung capacity
max volume of air in lungs
residual volume
air left in lungs after complete exhalation
vital capacity
air volume inhaled/exhaled in normal breath = tidal voume
VC = tidal volume + expiratory/inspiritory reserve
expiratory/inspiritory reserve
additional air forced out/inhaled
heart: blood flow order
vena cava > RA > tricuspid > RV > pulm valve > pulmonary A > lungs > pulmonary V > LA > bicuspid/mitral > LV > aortic valve > aorta
heart sounds
1st pump: AV valves close – RV contracts = pulmonary circulation
2nd pump: semilunar valves close – LV contracts = systemic circulation
electrical conduction in heart: order
SA node > AV node > bundle of His > purjunke fibres
cardiac output
CO = SV x HR
volume / min = (volume / beat) x (beats/min)
v-tach
heart beats too fast, cannot fill with blood, systemic pressure drops, no blood pumped
3 types of blood cells
- erythrocytes (RBCs) = EPO stimulates
- leukocytes (WBCs) – 5 types, granular vs agranular
- thrombocytes (platelets) = thromopietin stimulates
myogenic
no neurological input required
eg. HEART beating
granular leukocytes
neutrophils
eosinophils
basophils
agranular leukocytes
lymphocytes = B & T cells, mature different locations
monocytes = macrophages
blood typing
- blood type = which surface antigens your cells have, produce antibodies against what you don’t have
- AB = both antigens, NO antibodies (universal recipient)
- O = neither antigen, BOTH antibodies (universal donor)
- Rh factor = absence/presence of D allele, pregnancy issues for SECOND CHILD
blood pressure
- BP = gauage pressure (pressure above atmospheric)
- systolic = ventricular contraction, diastolic = ventricular relaxation
- pressure highest in aorta, largest drop in arterioles
- **ΔP = CO x TPR ** same as V = IR where ΔP is presure change in circulation (force), CO is current of blood, and total peripheral resistance (blood vessels = resistors)
- add more capillary beds in PARALLEL = decrease resistance total
- high resitance if longer and narrower vessels
hemoglobin dissociation curve
- hemoglobin = coopertive binding = s shaped curve
- “exercise is RIGHT”
- right shift = decrease affininty for O2 = favours unloading of O2 (in exercise) – high temp, high CO2, low pH shift RIGHT
- left shift = increase affinity for O2 = favours loading of O2 (eg. fetal hemoglobin)
CO2 in the blood
- CO2 travels as bicarbonate anion in the blood (SOLUBLE)
- CO2 + H2O = H2CO3 = H+ + HCO3-
hydrostatic vs osmotic pressure
hydrostatic pressure = PUSH = force of blood in vessels from heart, drops as fluid moves out of capillary
osmotic pressure = PULLS in = number of particles dissolved in plasma, if stays thre same, hydrostatic drops below osmotic and net flux of H20 IN
blood clotting
damaged vessel exposes collagen
thrombin is made, produces fibrin
fibrin forms net to catch RBCs
clot broken down by plasmin
complement system
nonspecific, proteins in blood
activated through antibody activation or without antibodies
interferons
if a cell gets infected by a virus, produces interferons
lowers permeability of nearby cells to protect them
increases MHC II molecules (extracellular)
MHC I / MHC II
MHC I = in all cells, for endogenous antigens (eg. virus)
MHC II = only on special APC’s for exogenous antigens (eg. bacteria)
macrophages
engulf + consume pathogens
MHC II
mast cells
release histamine
promote inflammation
ALLERGENS
NK cells
detects downregulation of MHC
destroys body’s own infected cells
dendritic cells
APC’s, present antigens to adaptive cells T/B
granulocytes
neutrophils, eosinophils, basophils
inflammatory response
cytokines and chemokines
cytokines = induce INFLAMMATION
chemokines = attract immune cells to site
B cells
- humoral immunity, mature in BM, exposure in lymph nodes
- plasma B cells = produce antibodies, tag cells for killing
- memory B cells = stay in lymph nodes
T cells
- cell-mediated immunity, mature in thymus
- CD4/MHC II - extracellular - HELPER T Cells (secrete lymphokines)
- CD8/MHC I - intracellular - CYTOTOXIC T Cells (inject toxic chemicals)
extracellular infection: process
- macrophages engulf bacteria, present bacterial antigens on MHC II, release cytokines
- cytokines attract inflammatory cells, mast cells release histamine, increase leakiness of blood vessels
- dendritic cells leave tissue to lymph node, presents antigens to B cells
- make plasma + memory B cells
- antibodies tavel to tissue, tag bacteria for destruction
- dendritic cells also activate helper T cells (recognize MHC II on APC’s)
intracellular infection: process
- infected cells produce interferons to protect nearby cells
- begin presenting viral proteins on MHC I
- CD8 recognizes MHC I antigens, injects toxin to kil
- if MHC gets downregulated by virus, NK cells detect this change
autoimmunity
- all cells in body express “self antigens” to signal immune cells not to attack
- autoimmunity where cells expressing self-antigens get attacked (eg. Beta cell destruction in T1D)
- can also have hypersensitivity to some foreign antigens (allergies!!!)
ADH and aldosterone trigger:
thirst
glucagon and ghrelin trigger
hunger
leptin & CCK trigger
satiety
enteropeptidase
master switch, secreted by duodenum
enteropeptidase activaqtes trypsin, which activates chemotrypsin and carboxypeptidase
brush border enzymes
most of the enzymes to break down di/tri/ biomolecules
enzymes for carbs, proteins, and lipids found here
DUODENUM lining
pancreas exocrine function
acinar cells make pancreatic juice, ezymes for all 3 molecules
pancreatic amylase, peptidases (trypsin, chemotrypsin, carboxypeptidase), lipase
all function in the duodenum
3 components in bile
- bile salts (like soap – polar + nonpolar) emulsify fats to allow lipase to break them down (lipase is polar!)
- pigments
- cholesterol
absorption of simple sugars and AA
absorbed by facilitated diffusion / active transport into epithelial cells
blood usescountercurrent multiplication to max absorption
cabrs + AA’s diffuse into capillaries, into liver via HPV
absorption of short chain fatty acids
follow the same path as sugar/AA’s – diffuse into capillaries
do not require transporters since nonpolar
absorption of large fats/glycerol/cholesterol
pass into epithelial cells, reform into triglycerides
packaged into chylomicrons – enter lymphatics via lacteals, to thoracic duct
absorption of vitamins
absorbed in small intestine
fat-soluble into chylomicrons
water-solubl follow AA/sugar into capillries
starling forces
high hydrostatic pressure in glomerulus forces fluid into capsule even though osmotic pressure is high in blood, hydrostatic pressure is higher
nephron structure
- descending limb = only permeable to water
- ascending limb = only permeable to salts
- DCT = aldosterone (reabsorbs Na+ and H2O)
- collecting duct = aldosterone + ADH (reabsorbs H2O)
osmotic vs oncotic pressure
osmotic pressure = sucking that draws water in due to solutes
oncotic pressure = osmotic P due to PROTEINS specifically
layers in the epidermins
- come lets get sun burned (top-bottom)
- stratum corneum
- stratum lucidium (only in thick, hairless)
- stratum granulosum
- stratum spinosum
- stratum basale
what’s found in epidermis
- keratinocytes
- langerhans cells (macrohpages)
- stem cells
- melanocytes (melanin)
what’s found in dermis
- sweat glands
- hair follicles
- blood vessels
- sensory receptors
what’s found in hypodermis
connective tissue
fat
thermoregulation: hot VS cold
- hot: sympathetic neurons, release of sweat, evap endothermic
- cold: arrector pilli muscles contract, shivering uses ATP, brown fat = decouples ETC to make HEAT
skeletal muscle: overview
- striated
- voluntary
- somatic
- MANY nuclei
- not myogenic (need NS input)
- red fibres, white fibres, sarcomere unit
smooth muscle: overview
- non striated
- involuntary
- autonomic
- 1 nuclei
- myogenic
cardiac muscle: overview
- striated
- invountary
- autonomic
- 1-2 nuclei
- myogenic
- intercalated discs, gap junctions
- sarcomeres like skeletal
red fibres
- skeletal muscle
- red = SLOW twitch, HIGH myoglobin, oxidative phos. for ATP
- contract SLOW but for SUSTAINED time
white fibres
- skeletal muscle
- white. =FAST twitch, LOW myoglobin, glycolysis/fermentation for ATP
- contract FAST but fatigue FAST
Ca+ and muscle contraction
- required for ALL MUSCLE contraction
- stored in the sarcoplasmic reticulum
- activated release by T-tubules
- Ca+ binds to sites on troponin, causes tropomyosin to REVEAL myosin binding site on actin
sarcomere structure
- THICK = myosin
- THIN = ACTIN + troponin bond to tropomyosin
- A band length does NOT change during contraction
- myofibrils = line of sarcomeres, surrounded by sarcoplasmic reticulum
sarcolemma
- cell membrane
- dsitributes action potentials to all sarcomeres using T-tubules
contraction STEPS: sarcomere
- neuromuscular junction, Ach released at synapse, binds receptors on sarcolemma = depolarized
- depolarization travels down T tubules to sarcoplasmic reticulum = Ca+ release
- Ca+ binds to troponin, changes tropomyosin to release myosin binding on actin
- myosin binds to actin (ADP state) – POWER stroke = RELEASE OF ADP, pulls filaments towards M line
- binding of ATP = release of myosin
- Ach degraded in synapse by enzyme, signal stops, Ca+ stops, binding sites covered, myosin binds ATP to release
rigor mortis
dead, no ATP, cant bind to myosin, so myosin cannot dissociate from actin (needs ATP to release)
STIFF
tetanus
- both disease and condition
- contractions so frequent that muscle cannot relax at all
- toxin blocks GABA that inhibits neurons, constant stimulation
- summation of muscle contractions until fatigue/failure
bone
- CT, mesoderm
- compact VS spongy (cavities with bone marrow)
- long bone: middle is diaphysis, ends are epiphysis
- bony matrix = structural unit, osteons
- most bones made by hardening of cartilage
epiphyseal growth plate
site of longitudinal bone growth
osteoblasts VS osteoclasts
- osteoblasts = make bone, activated by calcitonin (released by thyroid when Ca+ is HIGH to tone down Ca+), osteoblasts make new bone to lower Ca+ levels in blood
- osteoclasts = macrophage, resorb bone, stimulated by PTH to increase Ca+ levels in blood vitamin D promotes osteoclasts, which allows NEW bone to form
hemizygous
only ONE allele (eg. males hemizygous for X alleles)
penetrance
proportion of population with genotype that actually EXPRESSES it
expressivity
different phenotypes of the same genotype
griffith experiment
- transformation in mice + bacteria
- bacteria are capable of transferring genetic material = transformation
hershey and chase
- determined genetic info carried by nucelic acid by virus
insertion mutations
translocation mutations
insertion = DNA segment moved into a new chromosome
translocation = DNA segment of one chromosome SWAPPED for another
inborn errors of metabolism
defects in metabolism genes
eg. PKU = defect in Phe metabolism, cause toxic buildup
genetic leakage
flow of genes between SPECIES
genetic drift
founder effect
bottleneck
recombination frequency
likelihood that 2 alleles are separated (low = likely linked)
= proportional to distance between genes
hardy weinberg equilibrium
- population large, no mutations, random mating, no migration
- alleles: p + q = 1 (dominant allele + recessive allele = 1)
- PHENOTYPES: p^2 + 2pq + q^2 = 1 (homoz. dom + hetero + homoz. recess = 1)
genetic cross ratios:
PP x pp, Pp x Pp, Pp x pp
PP x pp = all Pp
Pp x Pp = 1 : 2 : 1 (PP:Pp:pp)
Pp x pp = 1 : 1 (Pp:pp)
dihybrid cross ratios: both heterozygous
9 : 3 : 3 : 1
x linked (sex)
men with trait CANNOT pass to their son
daughters are either carriers or have trait (if mother also affected)
modes of natural selection
- stabilizing selection = selects against extremes
- directional selection = adaptive pressures favour ONE extreme
- disruptive selection = favours BOTH extremes, not intermediate
speciation
formation of new species by REPRODUCTIVE ISOLATION
= progeny cannot interpreed, pre and post zyogtic mechanisms
structure of RBC
- no membrane bound nucleus
- no DNA
- no organelles
- just lots of hemoglobin
what amino acids get phosphorylated
Serine (S)
Tyrosine (Y)
Threonine (T)
mitochondrial DNA
inherited from MOTHERS
cytoplasmic DNA
single crossover VS double crossover events
- single crossover = affect only the ends of chromosome arms
- double crossover = middle of chromosome affected – chromosomal arms of homologous chromosomes cross over in two different places along the arm, results in a section in the middle of each chromosome being exchanged
analogous structures
Analogous structures are those structures that evolved independently to carry out the same function.
Thus, the wing of a bee and the wing of a bird are analogous structures.
homologous structures
Homologous structures are those that have a similar evolutionary history, arising from the same source, even if they now have different functions.
The forelimbs of mammals (human arm, walrus flipper, bat wing) would all be homologous despite their different functions
interneuron
intercommunication point for the afferent and efferent neurons within the CNS.
usually in spinal cord
number of possible gametes:
X = # of possibilities for each gene (usually 2)
n = number of genes total
X^n eg. 3 genes ABC and they are heterozygous for each, 2^3 = 8 combinations
