BIO 246 Study Guide for Exam I 

what are the cell basics?

Cell Physiology I

-Cell basics: plasma membrane, nucleus, organelles

 Ribosomes: Create proteins

 Rough Endoplasmic Reticulum: Produce and fold proteins

 Smooth Endoplasmic Reticulum: Produce hormone and lipids

 Mitochondria: Creates ATP

 Golgi Apparatus: Packages and sends out proteins

 Lysosomes: Contain enzymes that digest waste

-Homeostasis

 Internal equilibrium due to constant interplay within the cell when changes occur  in the external environment  

 Metabolism: Chemical reaction within the body

o Anabolic: Uses energy to build biomolecules including proteins, nucleic  acids, lipid, carbs

 Proteins made of amino acids

 Nucleic acids made of nucleotides

 Lipids made of fatty acids

 Carbohydrates made of monosaccharides(glucose)

o Catabolic: Release energy as it breaks down molecules

what is homeostasis?

 Chemical reactions:  

o Reversible: CO2 + H2O H2CO3 HCO3- + H+ 

o Need catalysts= enzymes= proteins

o Enzyme homeostasis depend on water, ions, pH,  

 Water: polar, solubilize ions, proteins, carbohydrates

 Cell membranes: made of amphipathic lipids- have hydrophobic tails and  hydrophilic heads  

o Creates semipermeable membrane: Only certain molecules can get through  Proteins: Can be polar & ionic, polar &uncharged, Non-polar.  

o Enzymes will denature with differences in pH, [Salt], temperature  pH scale: Pure water in neutral, pH=7 Don't forget about the age old question of Who is walter grove?

o Base: Absorb H+ ions, pH>7

o Acid: Release H+ ions, pH<7

Cell Physiology II

 Plasma membrane: phospholipid bilayer with proteins.  

 Membrane Transport

o Diffusion: Movement of solutes from high to low concentration. ALWAYS  PASSIVE  

 Passive: no energy required

what is catabolic?

 Simple diffusion: No channel/carrier protein, small nonpolar molecule-   Gases-Oxygen, Carbon Dioxide, Nitrogen

 Facilitated Diffusion: Molecule needs carrier or channel protein to get  across, passive

 Uncharged polar molecule- Water

 Large Uncharged polar molecule: glycerol, glucose

 Ions: Cl- ,K+ 

o Factors affecting Diffusion rate:

 Steeper concentration gradient, higher rate

 Higher SA, higher rate

 Higher Temperature, higher rate

 Small distance, higher rate

 Osmosis: Diffusion of water from low to high concentration of solutes, Passive,  “Water follows the salt”

o Isotonic: 2 solutions with same concentration of solute

 Isotonic extracellular: cell neither shrinks nor swells

o Hypertonic: solution with a greater concentration of solute than other  solution

 Hypertonic extracellular: cell shrinks (crenation)

o Hypotonic: Solution with lower concentration of solute than other solution  Hypotonic extracellular: cell swells (lysis) If you want to learn more check out ben haugland

o Osmolarity: # of particles contribute to the osmolarity when it solubilizes  200 mM NaCl= 400 milliosmoles. NaCl dissolves into two particles  Active Transport: facilitated (need membrane protein), moves molecules against  their concentration gradient, NEEDS ENERGY

o Primary Active Transport: Pump uses energy to pump molecules against  gradient

 Sodium/Potassium pump

o Secondary Active Transport: Energy derived from one solute moving down  its concentration gradient drives transport of another solute moving against  its gradient across the membrane

 Symport: Two molecules move the same way, Sodium and Glucose  Antiport: Two molecules move the opposite way, Sodium and Hydrogen  Saturation of Facilitated Transporters-both passive and active

o Rate of transport into cell is limited by number of carrier proteins in  membrane

o Diabetes: sugar in urine because of saturation of carrier proteins that usher  glucose into the cells

 Bulk Transport: Move big things, require ATP

o Endocytosis: internalize substances  

 Phagocytosis: cell eating

 Pinocytosis: Cell drinking

 Receptor mediated endocytosis- receptors recognize specific molecules  LDL, HDL

o Exocytosis: Moves vesicles carrying molecules out of cell, vesicles fuse with  plasma membrane, contents released  

Cell Physiology III

 Cells differentiate to have specific functions

o DNA RNA Protein  

Transcription Translation

 Cell phenotype is determined by types of proteins. Depends on types of genes  transcribed

 Transcription factors select genes from genome to differentiate cells  Tissue stem cells can replace damaged or dead tissues by differentiating o Self-renewal: makes copy of itself during mitosis, allows stem cells to not run  out If you want to learn more check out a logical view of how things work, and is frequently formulated on the basis of observation.

o Differentiate: another daughter cell differentiates and becomes functional  cell

 Levels of stemness

o Totipotent: Create any type of cell including placenta

o Pluripotent: Any adult tissue cells, not placenta

o Multipotent: Commit to a form a lineage of a tissue by some differentiation,  self-renewal

o Differentiated: Committed to function, no self-renewal

 Therapeutic potential: stem cells can be used to help treat diseases, bone marrow  transplants

o Adult stem cells: multipotent, hard to isolate, self-renewal, hard to isolate,  donor/host rejection

 Found among differentiated cells in a tissue/organ, daughter cells  differentiate

o Embryonic stem cells: pluripotent cell, can form ALL cells, donor/host  rejection

 Easy to expand and grow

 Most controversial: must destroy embryo in process

 Ethical dilemma

 Umbilical Cord stem cells could work in future

o Reprogrammed adult cells

 Somatic Cell Nuclear transfer: pluripotent, transfer adult nucleus into  an oocyte with DNA removed

 Issue of donor eggs & differentiating cells into needed tissue

 Ethical- clones

 No donor issue if own genome used

 Induced Pluripotent Stem Cells: 4 proteins were introduced to  

differentiated adult cells to reprogram them back to embryonic stem  cell state- Shinya Yamanka

 So promising because it is the person’s same genome and tissue  so no rejection possible

 Limits: Directing differentiation process is difficult into needed  Don't forget about the age old question of What is Cryptozoology?

tissue

Endocrine I

 Endocrine System vs Nervous System  

o Endocrine: slow, long duration, uses hormones in the blood to deliver  message, target cells have receptors intracellular (steroids) or on the plasma membrane (proteins, peptides)

o Nervous: fast, short duration, direct contact with target, synapse between  neurons

 Intercellular communication: Endocrine, Paracrine, Autocrine

 Endocrine Control Systems: Sensors detect changes in parameters and release  hormones, effector cells, target cells/organs to reestablish parameter back to  homeostasis

 Feedback Control: changing process of negative and positive feedback  o Comes from hormones, humoral nutrients, neurons

o Occurs at primary (peripheral gland), secondary (pituitary gland, tertiary  ( hypothalamus)

 Negative Feedback: Increase in parameter that leads to a change to decrease a  parameter, inhibiting of hormone release at all levels

 Positive Feedback: Increase in parameter causes an increase in parameter,  childbirth, ovulation  

 Hypothalamus: neurons are neurosecretory that release hormones into  hypophyseal portal blood We also discuss several other topics like utep cs

 Posterior pituitary: extension of neurons axons from hypothalamus, synapse on  blood vessels and release neurohormones  

o ADH- water balance, Oxytocin- reproduction We also discuss several other topics like these psychodynamic theorists give the greatest attention to the unified personality.

 Anterior Pituitary: fed by hypophyseal portal plexus full of hypothalamic releasing  hormones(-RH) and inhibiting hormones (-IH)

o Trope cells have receptors for -RH, that in turn release other hormones o Hypothalamus releases

 GHRH- growth hormone

 GHIH

 TRH- thyrotropin

 CRH- corticotropin

 GnRH (LHRH) -gonadotropin

o Anterior Pituitary releases

 GH- growth hormone

 TSH-thyrotropin stimulating

 ACTH-adrenocorticotropic hormone

 PRL-prolactin NO -RH IDENTIFIED

 Mammary glands

 FSH- follicle-stimulating hormone &LH- Luteinizing Hormones

 Stimulated release by GnRH

 Testes, Ovaries

Endocrine II

 Glucose Homeostasis

o Too much glucose cause tissue glycosylation where blood vessels can lose  elasticity

o Pancreas

 Islet cells that are sensory and regulatory

 Alpha cells: Release glucagon

 Beta cells: Release Insulin

o Low blood glucose causes the release of glucagon. Liver will break up  glycogen to produce glucose and start gluconeogenesis. Muscle will release  glucose from its glycogen stores. Fat cells will begin lipolysis to break down  fat to form fatty acids, glycerol, ketones for energy.

o High blood glucose causes the release of insulin. Liver will form glycogen,  stop gluconeogenesis and glycogenolysis. Muscle will increase uptake of  glucose to produce glycogen. Fat cells will increase uptake of glucose and  fatty acids to create triglycerides through lipogenesis.  

o Failed insulin signaling on the liver could cause an increase to  

gluconeogenesis. This would increase the glucose levels in the blood causing hyperglycemia- Type 2 diabetes

 Diabetes mellitus

o Hyperglycemia cause damage to nerves, blood vessels and eyes. o Type 1: insufficient insulin (pancreatic beta cells destroyed), juvenile onset o Type 2: insulin insensitivity, defect in receptor signaling, obesity  Insulin Receptor Signaling

o Insulin binds to receptor in membrane, signal transaction turns on GLUT  transporter

o Receptor is kinase: Enzyme that phosphorylates other proteins o Issues downstream proteins can be oncogenes- cancer cells

 Cortisol (Glucocorticoid): lipid, soluble steroid binds to nuclear receptors that act as transcription factors

o Regulation:

 Hypothalamus releases CRH

 Anterior Pituitary has corticotropes releases ACTH

 Adrenal Cortex releases Cortisol

o Target: Liver, muscle, adipose, brain

o Excess cortisol can suppress immune system

o Function: glucose and protein metabolism under long term stress o Related to glucagon: protein catabolism, lipolysis, glycogenolysis o Cushing Syndrome: excessive cortisol (tumor), muscle protein catabolized,  massive edema

o Addison’s Disease: rare, low cortisol, low blood sugar, low blood volume  Growth Hormone: soluble, polar peptide hormone, tissue growth, nutrient  metabolism

o Regulation:

 Hypothalamus releases GHRH/GHIH

 Anterior Pituitary has somatotropes release GH

o GH stimulates Insulin like Growth Factor (IGF-1) in the liver

o Causes increased protein synthesis and increased adipose breakdown o Receptors in cytoplasm- transporters

o Hyposecretion: little GH

 Children: dwarfism, stunted growth

o Hypersecretion: Excessive GH

 Children: Gigantism, tall

 Adults: Acromegaly- bones thicken (face and hands)- pituitary  adenoma (tumor)

 Thyroid hormone: water soluble

o Regulation

 Hypothalamus releases TRH (thyrotropin)

 Anterior Pituitary uses thyrotropes to release TSH

 Thyroid gland releases thyroid hormone (T3 AND T4)

o T3 and T4 created from Iodine atoms and amino acids  

o Regulates body temp through basal metabolism rate

o Responds to low body temp or metabolism

o Disorder

 Hypothyroid: goiter

 Iodine deficiency- goiter, can’t make T3 OR T4, too much TSH, no – feedback

 Hashimoto’s thyroiditis: autoimmune antibodies attack and kill  thyroid cells

 Hyperthyroid

 Grave’s Disease: autoimmune antibodies mimic TSH, too much  T3/T4, bug eyes, goiter

 Nodules- Thyroid cancer: too much T3/T4, carcinoma cells  

unresponsive to negative feedback

Reproduction: Male  

 Both sexes: Primordial germ cells develop fetus at 3 weeks post   Males: XY

o SYR (Sex Determining Region on Y Chromosome) encodes protein to signal  cells around to produce testosterone- masculinizes

 Females: XX

o Lack of testosterone leads to default pathway- develop uterus, ovaries,  vagina

 Puberty: Hypothalamic neurons reactive it

o Depends on body size, nutrient, energy

 Goals:

o Produce mature gametes- needs testosterone

o Develop Gametes through three E’s- need testosterone

 Erection, Emission, Ejaculation

 Erectile dysfunction corresponds with cardiovascular disease

 Secondary effects of Testosterone

o Maintain muscle mass, bone density, increased impulsiveness and  aggression, gonad formation

 Hormone Regulation

o Hypothalamus releases GnRH starting at puberty

o Anterior Pituitary has gonadotropes that release FSH and LH

o Produce Inhibin protein- inhibits FSH release

o Produce Testosterone- support sperm form

 Inhibits GnRH, FSH,LH release- negative feedback

o Pulsatile GnRH does not surge

o Constant GnRH shuts down LH secretion from gonadotropes

 Seminiferous Tubules contain:

o Leydig cells (interstitial)- steroidogenic, surround tubules

 Produce testosterone in response to LH  

 Testosterone negative feedback inhibits GnRH and LH release

 Testosterone acts on Sertoli cells

o Sertoli cells (sustentacular)

 Support spermatogenesis in response to FSH and testosterone  stimulation

 Produce inhibin- peptide hormone which inhibits FSH release

 Produce small amount of estrogen- provide nourishment and begin  meiosis

 FSH and testosterone needed for normal sperm production and  maturation

o Spermatogonia (diploid, 46 chromosomes)

 Stem cells going under mitosis and self-renewal

 Daughter cell enter meiosis to reduce to 23 chromosomes

 Meiosis 1- primary spermatocytes

 Meiosis 2- secondary spermatocytes

 Leads to spermatids maturing in sperm- haploid genome

o Sperm-motile cell, no X or Y

 Matures in epididymis

 Prostatic gland releases secretions in the semen that aid in sperm survival in  female reproductive tract

Reproduction: Female  

 Females: similar hypothalamic, pituitary hormones as males

o Differences: Target ovary, produce estrogen and progesterone

 Ovarian Follicles: oocyte surrounded by support cells

o Theca cells: respond to LH

 Produce androgen precursors to estrogen ( DHEA, testosterone)

 Become small luteal cells in corpus luteum

o Granulosa cells: respond to FSH, in basement membrane

 Express aromatase enzyme- convert androgens to estrogens

 Become large luteal cells in corpus luteum

o Oocyte- initial stage of meiosis

 Finish meiosis after ovulation and fertilization to haloid gamete cell  Estrogen to GnRH to LH surge restarts meiosis

 Ovarian cycle:

o Follicular phase: estrogen dominated

 LH and FSH stimulate high levels of estrogen production between theca and granulosa cells in follicle

 Estrogen stimulates hypothalamus to release surge of GnRH releases  LH (positive feedback)

 LH surge causes ovulation- follicle rupture and mature egg bursts out o Luteal phase: progesterone dominated  

 Corpus luteum produces progesterone and estrogen  

 No embryo: no hCG causes corpus luteum to self-destruct (luteolysis)  Embryo: secrete hCG- corpus luteum rescued

o LH & FSH use PKA Pathway

 LH activates GPCR (G Protein Coupled Receptor)

 Activates adenylate cyclase to produce cAMP

 Potent activator of PKA (kinas) that causes change in gene  

expression

 Uterine cycle:

o Proliferative phase: estrogen stimulates endometrial proliferation o Secretory phase: progesterone and estrogen stimulate endometrial  maturation/secretion

 Childbirth: includes oxytocin

 Lactation: include prolactin and oxytocin

 Oxytocin: binds to GPCR

o Activates PLC- causes DAG and calcium ions to flood the cell

o The calcium ion an lipid will activate PKC (kinase) that can change gene  expression

o Calcium also produces a muscle contraction