taxis
the movement of an organism in response to a stimulus
positive taxis
towards a stimulus
negative taxis
away from a stimulus
chemotaxis
the movement in response to chemicals (e.g. bacteria with flagella away from repellants or to nicer locations, neutrophils in humans with infection)
short-range cell-signaling
affects only nearby cells
long-range cell-signaling
affects cells throughout the organism
ligands
signaling molecules that bind to receptors to trigger a response by changing the shape of the receptor protein
ligand-gated ion channels
receptor that opens or closes an ion channel upon binding with a particular ligand
What are some examples of ligand-gated ion channels?
on skeletal muscle cells that open with acetylcholine; when sodium depolarizes muscle cells they contract
catalytic (enzyme-linked) receptors
enzymatic active site on cytoplasmic side of membrane (e.g. insulin receptors)
G-protein-linked receptor
no act as an enzyme, binds to GTP or GDP on intracellular side when a ligand is bound extracellularly
What is an example pf a G-protein linked receptor?
cAMP hunger signal activates the secondary messengers of epinephrine and glucagon
phosphorylation cascades
series of protein kinases add a phosphate group to the next protein in a cascade sequence, helps amplify signal, quickly turn response on or off
signal transduction in bacterial cells
usually a simpler two-component regulatory system in transduction pathways
signal transduction pathways can change stuff
cell's phenotype, apoptosis, mutations in receptor or ligand, drugs / chemicals inhibit or excite parts of pathway
negative feedback pathway (feedback inhibition)
when a metabolic reaction turns itself off using its own end product
cell communication in plants
signals in response to environmental stimuli, light receptors, chemical communication, between plants
non-dividing cells
often highly specialized cells created from a population of less specialized cells
temporarily non-dividing cells
enter G0 phase, where they stay until they get a signal to reenter the normal cell cycle
cell cycle
an orderly sequence of events that extends from when 2 daughter cells form to when they divide again
interphase
majority of cell cycle, metabolic activity = very high, chromosomes duplicated in S phase
G1 (growth 1)
before DNA synthesis begins, enzymes for S phase made (i.e. DNA helicase, DNA polymerase, DNA ligase), regular activity resumes, increased protein / organelle
S (DNA synthesis)
main part of chromosome duplication, DNA copied into sister chromatids
G2 (growth 2)
DNA synthesis completion, prepare for cell division, protein synth increased for proteins needed for cell division
mitotic (M) phase
most dramatic appearance changes, PMAT and cytokinesis
skin, digestive tract lining cells divide...
frequently, constantly sloughed off = must be regenerated
liver cells divide...
only if damaged (cell division repairs wounds)
nerve and muscle cells divide...
never
anchorage dependency
plant/animal cells must be anchored to a surface to divide (free-floating cells rarely divide)
density dependent inhibition
cells multiply to form single layer and stop dividing when touch each other because of inadequate growth factor supply
growth factors proteins
secreted by certain body cells, stimulate cells nearby to divide (more densely packed cells = more use up growth factors = divide slower)
cell cycle control system
cyclically operating set of proteins in the cell that trigger and coordinate major cell cycle events, from environmental conditions outside cell or go signals inside cell
cell cycle checkpoints
end of G1 (MOST IMPORTANT AS PREVENTS S PHASE) AND NON-DIVIDING STATE, end of G2 (prevents prophase / mitotic phase), metaphase (stops if not all chromosomes are attached to mitotic spindle on M plate)
cyclin dependent kinases (CDKs) and cyclins
bind to form a complex that causes the cell cycle to continue, regulated by checkpoints to control progression
carcinoma
cancer of external / internal body coverings (e.g. skin, intestinal lining)
sarcomas
cancer of supporting tissues (e.g. bone and muscle)
leukemias and lymphomas
cancers of blood-forming tissues (e.g. bone marrow, spleen, lymph nodes)
oncogenes
mutated genes that induce cancer, normally for proper cells growth and CCCS, but convert normal cells into cancerous cells due to mutated genes
proto-oncogene
normal healthy version of a gene
tumor suppressor genes
produce proteins that prevent the conversion of normal cells into cancer cells, detect damage in the cell, use CDK / cyclin complexes to stop cell growth until damage repaired
cancer causes
oncogenes (speed up cycle), tumor suppressors (remove stop checkpoints)
chemotherapy
antimitotic drugs disrupt cell division for whole body (vinblastine, taxol), fewer side effects
radiation therapy
direct to tumor high-energy radiation that disrupts division