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