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cell development include
- cell expansion, division, and death
- cell differentiation
cellular physiology
- ion and molecule concentrations
- metabolic activity
cell responses to external conditions
- directional growth in plants (phototropism, gravitropism)
- emotional responses in animals (high or flight, anxiety, arousal)
What do cell set of receptors allow?
respond to signal produced by other cells and by the environment
What is the role of an extracellular signal molecule in cell signaling?
Ligand is the signaling molecule that binds to the receptor.
What happens when a receptor protein is activated in cell signaling?
It initiates a signal cascade.
What is the function of intracellular signaling molecules in cell signaling?
They amplify and integrate the signal.
What do effector proteins do in cell signaling?
They carry out the cell responses.
what type of ligands bind to cell-surface receptors?
ligands that are too large and/or hydrophilic to pass through the membrane
what type of ligand binds to intracellular receptors?
small hydrophobic signal molecule that is able to pass through the membrane
What are the different classes of receptors?
1. transcription factor (cytoplasm/nucleus)
2. part of protein degradation complex (cytoplasmic)
3. ion channel (membrane-bound)
4. G protein coupled receptor (membrane bound, interacts with GTP-binding proteins)
5. membrane-bound enzyme (kinase)
example of a transcription factor receptor
Glucocorticoid receptor (hormone rector and transcription factor) when bound to the hormone cortisol, it becomes an active transcription factor and increases expression of a. number of genes that increase blood sugar levels and suppress the immune system
what type of ligand is the hormone cortisol?
hydrophobic membrane-soluble ligand that can pass through the plasma membrane and bind to glucocorticoid receptor, resulting in it moving into the nucleus and activating transcription
what hormone ligands are derived from cholesterol?
cortisol, estradiol, testosterone, thyroxine
what are the three classes of membrane bound receptors?
ion-channel receptor, G-protein-linked receptors, and enzyme-linked receptors
what do second messengers do in signal transduction pathways?
- they amplify and rapidly transmit the signal
- must be broken down or removed at some point, so that the signal is not left on
what are example of second messengers?
Cyclic AMP is derived from ATP
Cyclic GMP is derived from GTP
Ca2+ is removed from the cytoplasm and stored in the endoplasmic reticulum
Why is Ca2+ important in egg fertilization?
Multiple sperm reach the egg at the same time. When the first sperm penetrates the egg surface, Ca2+ is released from the endoplasmic reticulum. The released Ca2+ acts as a second messenger, changing protein activity that leads to structural changes at the egg surface that prevent other sperm from penetrating
Describe the cellular response to the hormone adrenaline
1. one molecule of ligand (adrenaline) binds to and activates the receptor
2. many molecules of the second messenger cAMP transmit the signal
3. cAMP activates a kinase, which in turn activates other proteins by phosphorylating them
4. glycogen breakdown by activated protein, releasing sugar for generating energy
important assets of cyclic AMP
- intracellular signaling molecule
- adenylyl cyclase forms cAMP from ATP
- adenylyl cyclase is activated (turned on) by a G-protein coupled receptor
- cyclic AMP phosphodiesterase deactivates cAMP
important aspects of adrenaline
- hormone is synthesized from the amino acid tyrosine by the adrenal glands
- rapidly released into the bloodstream upon stimulation
- "fight or flight" response (rapid heartbeat/breathing, release of energy stores in muscles, release of neurotransmitters that lock in memory)
what does the G protein coupled receptor do?
ligand binding to its receptor activates the G protein. The G protein activates adenylyl cyclase, which converts ATP to cAMP. cAMp activates a protein kinase, which in turn phosphorylates proteins to turn them on
how is cAMp deactivated?
cyclic AMP phosphodiesterase breaks down cAMP to turn off the pathway (ex. to turn off the "fight or flight" response)
What is Anaphylaxis?
- severe allergic reaction (ex. nuts, seafood)
- symptoms: rapid tongue and throat swelling, unconsciousness and death
- adrenaline from the EpiPen dilates airway passages to the lungs and constricts blood vessels to alleviate shock symptoms
What is the role of rods in the retina?
Rods are cells within the retina that contain rhodopsin, which absorbs (senses) light.
What happens when rhodopsin in rods senses light?
Light sensing by rhodopsin leads to the breakdown of the second messenger cyclic GMP.
How does the breakdown of cyclic GMP affect rod cells?
When cyclic GMP is broken down by a phosphodiesterase, Na+ channels rapidly close, changing the membrane potential of the rod cell.
How does the membrane potential change in rod cells affect vision signal transmission?
The membrane potential change affects neurotransmitter release, allowing neurons to relay the vision signal to the brain.
smell depends upon G-protein-linked receptors
cAMp opens membrane Na+ channels nerve cell becomes depolarized (signal sent to brain)
endocrine system cell to cell signaling in animals
distant targets, widely distributed ex. hormones usually carried by the blood to target
paracrine system cell to cell signaling in animals
close targets, adjacent cells or a few cells apart ex. interleukins, growth factors, nitric oxide etc.
neurotransmitters cell to cell signaling in animals
highly directed release ex. dopamine, serotonin, acetylcholine, etc.
contact-dependent cell to cell signaling in animals
ligand remains attached to signaling cell ex. important for regulating cell differentiation during development
What is the role of nitric oxide in blood vessels?
Nitric oxide causes smooth muscle relaxation, leading to blood vessel dilation and increased blood flow.
How is nitric oxide produced in blood vessels?
An enzyme in endothelial cells acts on arginine to produce nitric oxide when neurotransmitter signals are received from the brain.
What happens to smooth muscle cells in blood vessels when nitric oxide binds to guanylyl cyclase?
Smooth muscle cells relax, leading to blood vessel dilation and increased blood flow.
Angina
severe chest pains due to the constriction or blockage or coronary arteries (not enough oxygen gets to the heart muscles, which causes the pain) and a symptom of cardiovascular disease
angina treatment
nitroglycerin which gets metabolized by cells releasing nitric oxide; nitric oxide travels through the bloodstream and acts as a ligand (binding to receptor in blood vessel smooth muscle cells, signaling them to relax, which allows more blood flow to heart muscle)
mechanism of erection
- when sexually aroused neurotransmitters signal nitric oxide formation in blood vessel endothelial cells
- nitric oxide binds to guanylyl cyclase, which converts GTP to the second messenger cGMP
- cGMP turns on kinases that turn on Ca2+ transporters in the endoplasmic reticulum, pumping Ca2+ out of the cytoplasm
- low cytoplasmic Ca2+ levels result in smooth muscle relaxation and blood flow into the penis
cardiovascular erectile dysfunction
- The penis becomes erect when smooth muscles of arteries entering the penis relax. This dilates (opens) the arteries, allowing blood to fill the penis (erection)
- If the arteries feeding the penis are hardened or clogged, smooth muscle relaxation does not open the arteries enough to "get it up"
Viagra and Cialis help ED
inhibit the enzyme phosphodiesterase 5 (PDE5). PDE5 breaks down the second messenger cGMP in blood vessel smooth muscle cells, With no PDE5 activity, the cGMP signal stays strongly on, which keeps the smooth muscles from contracting and restricting blood flow to the penis
receptor kinase signal transduction pathway
- common pathway type in eukaryotes and prokaryotes
- kinase activity of the receptor gets turned on when a ligand binds
receptor kinase signal transduction pathway in plants
- ligand is the diffusible gas ethylene
- involved in fruit ripening, flower development, and the etiolation response (a light response)
totipotent stem cell
a cell that can divide and produce all the differentiated cells in an organism
pluripotent stem cell
a cell that has the potential to differentiate into ay of the 3 germ layers; endoderm, mesoderm, or ectoderm
multipotent stem cells
cells that can give rise to a limited number of other cell types
tissue renewal
- replacement cells in a given tissue are derived from adult stem cells (multipoint or unipotent stem cells)
- apoptosis (programmed cell death) is essential for disposing of old and damaged cells and for maintaining proper cell numbers
what happens if there is an imbalance between cell division and apoptosis?
- tissue thinning: not enough new cells to replace dying or sloughing off cells. ex. with old age, skin thins, bones become pores, brain cells die from lack of use or disease
- tumor formation
skin cell turnover and damage
- as you age, skin basal cell division slows down and your skin gets thinner
- mutations induced by ultraviolet light from the sun cause defects in skin cell pigmentation, function, and cell division regulation
blood cells all derive from hemopoietic stem cell
- one stem cell type gives rise to many different blood cell types
- red blood cells (erythrocytes) survive about 120 days
- more than 2 million red blood cells are generated in your body every second
- the worn-out and damaged blood cells are recycled in your spleen
- a healthy person can donate blood every 56 days
What are hepatocytes?
Liver stem cells that can differentiate into all liver cell types.
How do old and damaged liver cells die?
By apoptosis within 300-500 days.
What makes the liver unique in terms of regeneration?
It is the only internal human organ capable of natural regeneration of lost tissue.
Osteoporosis
- bone disease common in older women (weak bones that fracture easily) bones are constantly remodeled; occurs when bones break down faster than built up
- how to prevent: take calcium and vitamin D supplements throughout life, perform weight bearing exercise, hormone replacement
What do checkpoints assess in cell growth and division?
- cell environment (extracellular signals saying the environment is favorable and/or it's time to divide)
- DNA replication (make sure replication is complete and DNA is not damaged)
- cell size (if too large or too small, have a selective disadvantage)
- proper cell contents ( enough energy molecules, organelles, etc.)
- paper chromosome attachment to mitotic spindles ( chromosome loss leads to cell death or other malfunctions including uncontrolled division)
cell cycle is controlled by
1. signal that induce growth which include Environmental and developmental
2. signals that halt growth which include environment conditions not being favorable and cell growth criteria not being met
What regulates the cell cycle?
Protein kinase called Cdk's (cyclin dependent kinases)
What are cyclins?
Proteins that must bind to Cdk proteins for activation
How do M-cyclin levels affect the cell cycle?
Rise throughout interphase, reaching a high concentration for M-Cdk activation, leading to mitosis
What happens to M-cyclin at the end of mitosis?
Targeted for protein degradation (proteolysis), deactivating M-Cdk and sending the cell into interphase
necrosis
premature cell death due to infection, toxins, or trauma. cell contents are released, which elicits inflammation and damage to surrounding cells/tissue. surgical removal necessary if extensive
apoptosis
programmed cell death. cell contents are destroyed in a controlled manner (plasma membrane does not rupture so no damage occurs to surrounding cells) DNA is fragmented and organelles and proteins broken down. dead cell material is recycled by phagocytosis
why do eukaryotic cells undergo apoptosis?
- critical for development (sculptures tissues and organs)
- gets rid of old/worn out cells as part of tissue regeneration (liver cells are replaced regularly)
- destroys malfunctioning cells (precancerous cells)
cancer
- a tumor is any abnormal growth of cells or tissue. tumors can be benign or malignant
- cancers are generally malignant tumors which grow rapidly and can metastasize
- not contagious
benign tumors
don't spread to other parts of the body, and are rarely life-threatening
malignant tumors
spread by direct invasion of neighboring tissues, and also by releasing cancer cells into the bloodstream
What is metastasis?
1. cancer cells invade surrounding tissues and vessels
2. cancer cells are transported by the circulatory system to distinct sites
3. cancer cells reinvade and grow at new location
what are the general cancer cell characteristics?
1. defensive in proper signaling; not responsive to external or internal signals
2. defective in apoptotic pathways
3. immortal (divide indefinitely like stem cells due to defects in cell cycle check points)
4. generically unstable (widespread chromosomal rearrangements and mutations)
5. invasive (able to migrate throughout the body from site of origin)
6. thrive in other tissues (metastases)
What is the sensing mechanism in cells?
Cells in contact with each other sense each other and inhibit each other's growth.
What happens if sensing mechanism in cell is defective?
Defective cells will continue to grow due to mutations, potentially leading to precancerous or cancerous growth.
cells become invasive when mutation occur in pathways affecting cell migration
- metastatic cells travel through the bloodstream and often times end up in the liver
- most cancer cells die when they migrate, but a few get established and grow (metastasis)
genomic instability characteristics cancer
somatic mutations leads to proliferation leads to more mutations leads to genomic instability
cancer cells may have one or more of the following traits
1. missing or extra chromosomes
2. multiple chromosomal translocation
3. defective DNA repair pathways leading to excessive mutations
mutagens (environmental and endogenous)
- cigarette smoke is a major cause of lung cancer
- UV light (from the sun) is a major cause of skin cancer
- oxidative damage (normal cell metabolism; being overweight)
- carcinogenic chemicals (charred meat from grilling)
- cosmic radiation, x-rays, nuclear power plant accidents
hereditary (inherited mutations)
- BRCA 1 and 2 gene (predisposition for great and ovarian cancer)
- HNPCC gene (80% lifetime risk for colon cancer)
- gene causing xeroderma pigmentosum (predisposition for skin cancer)
viruses
- HPV (cause cervical cancer)
- epstein-barr virus (cause lymphomas)
- hepatitis B and C (cause liver cancer)
when doe malignancy occur?
only after a number of mutations affecting cell proliferation, survival, and invasion accumulate in a given cell
where can stem cells a rise from?
intestinal epithelial cells are some of the most active cells in the body
colon cancer involves stepwise mutational events starting with adenomatous polyposis coli (APC)
1. normal epithelium (tumor suppressor gene APC lost)
2. excessive epithelial proliferation (oncogene Was activated)
3. small tumor (another tumor suppressor gene lost)
4. large tumor (a third tumor suppressor gene p53 lost)
5. tumor becomes invasive (rapid accumulation of mutations)
6. metastasis
why do all cancers require multiple mutations to accumulate before uncontrolled cell proliferation occurs?
cell growth has many check points and If only one growth signaling pathway is mutated, other checkpoints put a halt to uncontrolled growth
cancer prevalence in your lifetime
- mutations in your genes occur continuously over you lifetime
- incidence of cancer rises sharply in older people because that is how long it usually takes for the right combination of mutations to accumulate in a given cell
example of cell growth pathway that when altered can result in cancer
- the Wet signaling pathway regulates proliferation of intestinal epithelial cells
- the APC protein inhibits a transcription activator when the ligand Went is absent
- upon Want binding to its receptor, APX is inactivated, which allows the transcription activator to turn on transcription of genes leading to cell proliferation
- APC is called a tumor suppressor protein because it normally suppresses cell growth
- non-functional APC protein results in the Wet signaling pathway being constitutively (always) on resulting in cell proliferation even when the Wnt signaling ligand is not present
- mutations in APC can result in colon polyps or cancer
- APC is called a tumor suppressor protein because it normally suppresses cell growth
breast cancer incidence
- women have 1 in 8 chance of having breast cancer in their lifetime
Why is it that most prevalent for women in their 30's and 40's to get breast cancer and ovarian cancer ?
genetic predisposition
- some women are born with mutations in either the BRCA1 or BRCA2 gene (tumor suppressor genes)
- nonfunctional BRCA1 and BRCA2 results in great and ovarian cells rapidly accumulating mutations (chromosomal rearrangements) cause aging as well as tumor formation at an early age
what is the link of junk food and cancer?
a high sugar diet increases glycolysis in cells producing a metabolite (methylglyoxal; MGO) that can doable the tumor suppression gene BRCA2 which can increase DNA damage and cancer risk
early detection of breast cancer
- yearly mammograms starting at age 40
- clinical breast exam every 3 years starting at age 20 and 30
- early 20's do self treat examiantions
How many known types of Human papillomavirus (HPV) are there?
200
What cells does HPV affect?
Skin epithelial cells and mucous membrane cells
What are some conditions caused by HPV?
Skin warts, genital warts, cervical cancer, oral, penile, anal, and vaginal cancers
What percentage of cervical HPV infections can develop into precancerous lesions?
5-10%
What is the recommended screening method for cervical HPV infections in women?
Regular Pap smears because they can detect infected cells before they become cancerous
Why is the HPV vaccine (Gardasil or cervarix) recommended for men and women?
- receive between ages 9 to 26
- guardrail protects against 4 HPV types that are responsible for 70 % of cervical cancer cases and 90% of genital warts cases
how long does to take for HPV infection to turn into cancer?
10 to 20 years
how to limit your risk of cancer?
- stay away from tobacco
- get vaccinated against HPV
- protect your skin
- stay at a healthy weight
- get moving with regular physical activity
- eat healthy with plenty of fruits and veggies
- limit alcohol intake
- know family history
- regular check ups
how are cancer cells killed with surgery?
physically remove tumor (most affective prior to metastasis)
how are cancer cells killed with radiation?
gamma rays are focused on the tumor
how are cancer cells killed with chemotherapy?
hundreds of toxic drugs are used, many of which preferentially target actively dividing cells (cause DNA damage, cell cycle arrest, anti-angiogenesis, anti-metabolite)
how are cancer cells killed with immunotherapy?
tag the cancer cells with molecules that will elicit an immune response against those cells (interferons, cytokines, antibody molecules)
chemotherapy
- different drugs are used for different cancers, at different stages of the treatment and in conjunction with how well the patient responds
cancer drug examples
1. cisplatin (apoptotic; binds to and crosslinks DNA causing apoptosis)
2. paclitaxel taxol ( anti mitotic; stabilizes microtubules and inhibits cell division)
3. 5-fluorouracil (antimetabolite; blocks synthesis of the DNA base thymidine)
