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backevia present... → larger amount of AHL produced it all levels get high mough, indicating evitical density of bacteria, all will bind to & activate positive feedback loop - product of a reaction leads to an increase in that reaction ·bachria has auhinducer & highly specific receptor biofilm- surface - attached communities of bacterial cells that stick to one another & to their substrate cell-cell junctions plasmodesmata- places where a hole plasmodesmata * ·molecules below a connexon cerloin size-passive diffusion through plasmodermata plasmodesmate may selectively dilate to allow passage of certain large mokinkes gap juctions - like plasmodesmata in animal celli - channels between neighboring cells allows transport of ions, H₂O, ck. in verk brakes gap junctions develop when 6 membram prohing called connexions form a donut-like structure called a when is punched in the cell wall to allow direct cytoplasmic exchange between two cells cell wall - cytoplasm - pathway -vacnok - through cykeplasm connexion pores align, a channel forms between colls light juctions - evente a water light seal between to adjacent animal cells of tight juction proteins clauding individual groups - interact w/ parlour groups on → strands arranged to form a • purpose of light junctions: keep liquid from escaping between cells receptor protin opposite cell membrane branching network desmosomes in animal cells - act like spot welds between adjaunt epithelical cells and having adhesion proking found the membranes of both cells & interact in inside, andhaving attach to vyleplasmic plaque which anchors junction. •desmosomes pin adjacent cells together ensuring that cells in organs. on inside of cell - involves a complex of proteins space between, holding them together & Lissues shelch & remain unbroken ligands & receptors intracellular receptors - receptor proking on ↳ usually ligands are small & hydrophobic hormone binds to recepter - changes its shape - receptor - hormone complex entus nuckus - on outside surface of sells cell-surface receptors - bind to ligands 43 domains: enzyme- linked receptors - cell-surface receptors - intracellular domains - extracellular - outside of cell hydrophobic throughout membram intracellular - inside of cell ligand-gated son channel - ion channels that can open in response to binding of a ligand I prohin- coupled receptors - large hamily of receptors - share structure & method of signaling all bind GTPhydrolyze GDP GTP a Hached = active GDP attached = inactive regulates gone activity associated w/ enzymes signal relay pathways upstream - describe molecules & events that came earlier in the relay chain downstream those that come later phosphorylation : -alters prokin activity w/ addition of a phosphate group - transfer of phosphate group is catalyzed by kinase - phosphatases - flip proking back to this non-phosphorylated state second messengers - small, non-prokin molecules - pass along Sex: calcium ion) GPCRs: -span membrane 7 times - all goproteins associated w/ GPCRs are hetero trime chic alpha, beta, gamma subunits • conformational change after ligand binds alpha subunit exchanges GOP for GTP alpha subunit disociates & regulates target prokin signal via second messenger torget protein relays - GTP hydrolyzed to GOP example: adrenaline - is break down glycogen gleose for energy a adhaylate cyclase regulated. response to a signal molecular level : increase in wanscription of certain gimus macroscopic level. cell growth gine expression. avanscription makes and copy of on a transduction reads into from ana a - produce came from ATP 2nd messenger to make or death caused by molecular changes signal initiated by the binding of a ligand to its receptar a protein. growth factor pathway offects gene expression in translation 3 • promotes cell growth & division • epinephrine (adrenaline) triggers activation of glycogen phosphorylase & the breakdown of apoptosis programmed cell death homeostasis homeostasis-tendency to resist change in order to maintain a stable, relatively constant internal environment. in blood skeady to prevent sickness & body maintains temp., pH, & concentration of various ions maintain function negative feedback loops: · act to oppose the stimulus that triggers them back toward a set point 2. high temp. directed by rensors 2. relayed to temp- regulatory control center in brain 3. control center activates ettectors who appose stimulus ( aka - hypothalamus body temp. falls • body timp. rises 50 heat is retained heat lost to the environment blood vessels constrict so that is consered, sweat glands do not server fluid, shivering generates heat which warms the body normal body smp. blood vessels dilate - resulting in wat 1035 to the environment, sweat glands secrete fluid - fluid evaporates - heat is lost from the body - drabetes - caused insulin decreases the blood glucose concentration be causes glucose to -glucagon - increases glucose concentration in blood La breaks glycogen into glucose glycogen by a broken feedback loop involving the hormone insulin be converted to glycogen. • positive feedback loops amplify the storking signal ex: childbirth - ex fruit ripening hormone oxytocin amplifies contractions cell cycle eukaryotic cells do... interphase - cell grows & makes a copy of its on a mitotic phase - cell separates its on a into two rets & divides it's cytoplasm ENTER PHASE: G phase M PHASE: 6² phase - cell grows larger, copies organelles, & makes molecular building blocks for later steps s phase - cell synthusizes a complete copy of Ona in its nucleus, duplicates centrosome which help separate ona during M phase cell grows move, makes proteins & organelles, begins to reorganize contents in prep. for mitosis mitosis - Ona condenses into chromecomes & is pulled apart by mitotic spindle - specialized structure made of microtubules-takes place in prophase, metaphase, anaphose, & telophase cytokinesis- cytoplasm of cell is split in in animal tells.... two • contractile ving contracts inward & pinches the rell in • cleavage furrow - indentation produced forming two new cells in plant cells ... • divide in two by building a 6° phase - cell not preparing to divide - its doing its job two (contractile cytokinesis) as the ring contracts inward cell plate down the middle FARLY PROPHASE: -chuemosomes start to condense • mitotic spindle begins to form to Cits job is to organize the chromosomes ] spindle grows between the • aucleolus disappears LATE PROPHASE / PROMETA PHASE: · chromosomes METAPHASE: become even more compact nuclear envelope breaks down • mitotic spindle grows more kinetichore microtubules microtubules that bind a chromosome centromeres regions of on a where sister chromatics are anaPHASE: 0 SELET spindle checkpoint. is assures centrosomes aster chromosomes as they move apart some microtubules start to -Kimitochore microtubule of • all chromosomes align at the metaphase plate · two kintachoves should centromere kinetochore "capture" chromosomes sister chromatids will be split evenly most tightly connected. be attached to microtubules from opposite spindle poles cell will chuck to maku sure chromosomes will • sister chromatids separate - pulled toward opposite ends of the cell • microtubules separate poles & malu cell longer motor prokins - molecular machines that can "walk" along microtubule or other microtubules carry line up correctly tracks & carry a cargo. TELOPHASE: • mitotic spindle is broken down new nuclei form · chromosomes decondense (stringy form) chromosomes • humans have 46 chromosomes. 4 humans are diploid- most chromosomes come in matched pairs Chomologous pairs) & egg cells are haploid homologous pales carry same type of genetic info autosomes - 44 non-sex cells sperm cell cycle check points checkpoint - stage in eukaryotic cell cycle at which or not to move forward w/ division. . the rell examines internal & external cues & "decides" whither most important checkpoints.... cell sou Antrients · Gy checkpoint Gy /5 transition - primary point in which cell decides whether to dividh chicks: - growth factors a damage ona damage G₂ checkpoint G₂/M transition - makes suve division goes smoothly I checks: - on a replication completeness spindle checkpoint metaphase / anaphase transition. examines whether all sister chromatids are correctly attached to the spindle microtubules • internal & external cuis trigger signaling pathways inside the cell that activate, or inactivat the cell cycle forwand that move a set of care proting cell cycle regulatory cyclins (Gy cyclins, G₁/5 cyclins, 3 cycling, in eyelins) - group of related proteins that drive the events of a phase cyclin expression cycle 6₁/5 chelsn It Gy cyclin s phase G₁ phase 'S cyclin On 6₂ phase I'm cyclin 2. triggers production of colk inhibitor (CKI) proteins. 3. CK/ proteins stop cdk-cyclia complexes to make M phase. - to drive cell cycle, a cyclin must activate or inactivate many target proking inside the cell is partner w/ a hamily of enzymes (eyelin-dependent kinases or (dles) ·calks are enzymes that phosphorylate torget proking adding phosphate group can · maturation - promoting factor - example of how cyclins & Colks work together to drive cell cycle transitions 1. M cyclin accumulaks 2. binds w/ calks to form complexes that wigger in phase. 3. mps complexes add phosphate togs to protesus in the nuclear envelope causing it to break down 4. triggers own destruction by activating anaphase - promoting complex / cyclosome ·apc/c causes distruction of proking holding sister chromatids together allowing them to separate to opposite poles ·are / add small protein tag (ubiquitin Ub) to meyclins - distroyed by proteasome - allowing newly fourning daughter cells to enter by phase - apc/c uses ubiquitin logging to trigger the separation of sister chromatids during mitosis (distroys colusion) · p53 ensures that cells do not pass damaged Ona 1. stops at Gy checkpoint · 69 cycline needed throughout. cell cycle time for on a repair cyclin increases at the stage where it is meded - otherwise it exists at low levels binding allows it to modity target groteins make the prokain more or less active 4. activates on a repair enzymes S. if ona is not fixable, p53 will trigger programmed cell death. prevents mutations in daughter calls that could lead to cancer cancer be the cell cycle cancer disease of uncontrolled cell division • cancer cells can make their own growth factors, have growth factor pathways that stuck on wick mighboring cells into producing growth factors to sustain them. replicative immortality cancer cells divide many more times to because of the enzyme kelomerase which reverses the wearing down of chromosome ends metastasis- cancer cells gain the ability to migrate to other parts of the body. angiogenesis cancer cells promote the growth of new blood vessels which gives tumor cells most cancers as cells acquire a series of mutations that allow them to device quickly, escape internal & extemal controls on division, & avoid programmed cell death. source of oxygen & nutrients benign tumor- mass of cells that divich too much but do not have the potential to invade other malignant tumor group of cells that divich excessively & can invade other tissues. - it a cell nonfunctional genome stability factor its descendants may meded for cancer much faster than normal cells than proto-oncogens · normal body cell promotes development of oncogens overactive, cancer- promoting forms of gives not-yet-mutated forms fumor suppressors - gines that normally block cell cycle progression reach the "on" position, or tissuas the critical mass of mutations cancer: positive regulateus overachuated & regative regulations inactivated 5 pooto-oncogene oncogern through amplification - cell gains extra copies of a gove causing it to make too much postion