AP Bio Unit 4 Communication

direct contact

communication through cell junctions; ligands dissolve dint he cytoplasm can pass between adjacent cells

direct contact (examples)

gap junctions and plasmodesmata

juxtacrine signaling

short distance signaling where ligands are membrane-bound; direct “cell-to-cell communication”

local regulators

chemical messages released by secreting cells; travel through extracellular fluid

paracrine signaling

short distance signaling where cells use exocytosis to secrete ligands; “cell A secretes a ligand to cell B nearby“

autocrine signaling

cells receives the ligand that they produce themselves

long distance signaling

chemical signals travel via bloodstream

long distance signaling examples

plant hormones, endocrine signaling in animals (insulin, growth hormone, testosterone, estrogen)

cell signaling process

reception → transduction → response

reception

ligand binds to receptor; receptor are mostly extracellular but there are intracellular receptor

conformational change

a change in shape; how a receptor is activated

receptor locations

extracellular: plasma membrane; intracellular: cytosol, nucleus

transduction

conversion of an extracellular signal into intracellular signal; signal changes form to elicit cellular response

protein kinase

adds the phosphate group

phosphotase

dephosphorylates the protein

phosphorylation cascade

unites inorganic phosphate to a molecule

second messengers

small non-protein molecules and ions that do not initiate but amplify signal transduction

second messenger examples

cAMP, IP3, Ca2+ ions

GPCR

G protein-coupled receptors; extracellular ligand receptor with 7 subunits; G protein binds to a GTP and causes conformational change, part of G protein detaches and activates enzyme, synthesizing cAMP

ligand gated ion channel

on the plasma membrane; ligand binds to receptor, initiates the diffusion of specific ions; NOT ion pumps

RTK

receptor tyrosine kinases; dimer with inactive domains; dimer joins together when activated; needs enough P for two transduction pathways

What do signal transduction pathways influence?

how cells respond to their environment; may result in changes in gene expression and cell function

quorum sensing

bacteria release signals to neighboring bacteria; as bacteria pop. increases, signal are produced and all bacteria respond until a limit is reached; used to detect changes in pop. density

apoptosis

programmed cell death; can be triggered by ligand, DNA damage, protein misfolding

apoptotic bodies

vesicles that are produced in apoptosis; will be absorbed by other cells by phagocytosis

mutation in transduction pathways

can disrupt downstream signaling in the transduction pathway; can happen in any step of the pathway

feedback

processes that (try to) maintain homeostasis

homeostasis

maintenance of a stable internal environment; dynamic balance

negative feedback

returns the system back to set point

negative feedback examples

blood pressure, CO2 regulation

positive feedback

drives the system away from the set point; may be vicious but may also maintain homeostasis

positive feedback examples

heart rate increase during blood loss (-); oxytocin increase during childbirth (+); oxytocin increase during lactation (+)

nucleosomes

1 histone with genetic information

chromatin

packaged form of nucleosomes in the nucleus; stays this form in G0 phase

chromosome

condensed form for cell division

sister chromatid

same gene, same allele, duplicated counterpart during cell division

kinetochores

part that attached 2 sister chromatids together post-duplication in the centromere

genome

all of the DNA of an organism

cell cycle

interphase (G1 → S → G2) → M phase (mitosis → cytokinesis)

interphase

newly divided cells grow, maintain normal cell function, and prepare for cell division

G1 phase

cell growth

S phase

copying of DNA; “S” for synthesis

G2 phase

cytoplasmic components are doubled

somatic cells

diploid cells that divide by mitosis

gametes

haploid reproductive cells that divide by meiosis

diploid

2n; 2 sets of chromosomes, one set form each parent

haploid

n; one set of chromosomes

mitosis phase product

two identical diploid daughter cell

prophase

chromatin condenses; nucleoli disappear; mitotic spindle begins to form

prometaphase

nuclear envelop fragments; microtubules attach to kinetochores

metaphase

chromosomes line up at “metaphase plate;” centrosomes arrive at opposite poles of cell

anaphase

sister chromatids separate and dragged to opposite ends; microtubules shorten and dissolve

telophase

two daughter nuclei form; nucleoli reappear; chromosomes less condensed

cytokinesis

cytosol splits; happens simultaneously with telophase

G1 checkpoint

checks for DNA damage, cell size, growth factors

G2 checkpoint

checks for completion in DNA replication and DNA damage

M-spindle checkpoint

checks for nondisjunction and attachment of microtubules to kinetochores at metaphase

nondisjunction

incorrect separation of sister chromatids

cyclins

proteins that regulate cell cycle; concentration fluctuates; produced to promote cycle progression and degraded to inhibit progression

Cdk

cyclin-dependent kinases; conc. stays the same throughout; phosphorylate substrates

MPF

mitosis promoting factor, which is a cyclin-Cdk complex

result of disruption in cell cycle

cancer and/or apoptosis; can be caused by DNA damage or protein misfolding

proto-oncogenes

normal, healthy genes that regulate cell growth, division, and survival

oncogenes

mutates or overexpressed proto-oncogenes that causes uncontrolled cell duplication => cancer

tumor suppressor genes

gene that suppress tumors and protect the cell cycle’s function

anchorage dependence

cells rely on attachment to other cells

confluency

mitosis also regulated by density-dependent inhibition