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Test 3 Study Notes.docx

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Department
Chemistry
Course Code
CHEM 1001
Professor
Hernan Humana

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TEST #3 BIOLOGY 1000 STUDY NOTES Persephone Greco-Otto CHAPTER 8: CELL COMMUNICATION  Cells need to communicate with each other to make things happen (eg. muscle contraction neurons and muscle cells communicating) cell communication  response/event  Dictyostelium discoideum (slime mold) o Single cell amoeba, lives in soil/dead plant material o When food scare they aggregate (cells attracted to each other using cell-to-cell communication  single cells combine to become multicellular) by releasing a chemical into extracellular environment that’s detected by others and move towards  Extracellular Signaling = communication BETWEEN cells o Direct Contact = communicating cells attached/touching  Communicate via gap junctions in animals cells, plasmodesmata in plant cells  Cell-Cell Recognition = cells touching + recognize/communicate via extracellular protrusions (eg. proteins) o Local = communicating cells situated NEAR each other o Long Distance = communicating cells situated far away from each other  For BOTH local and LD, chemicals released by SIGNALING CELL are detected by RECEPTORS (integral proteins w/extracellular binding site) on TARGET CELLS  Eg. acetylcholine released from nerve cell, binds to receptor on muscle cell = muscle contraction (response)  Hormones = released by endocrine cell into blood, eg. growth hormones[in plants  travel in vessels, through cells and air eg. ethylene travels through cells/air + initiates growth/ripening  Steroid Hormones = small, nonpolar, passively diffuse through membrane, bind to receptors on nucleus, leads to gene regulation eg. testosterone  Signaling Molecule-Receptor Interaction o Chemical released by signaling cell = signaling molecule (must bind w/associated receptor to initiate a response  if no fit, no response)  Signaling + Target Cells o Cells can receive + release chemicals (can be signaling [releasing] + target [receiving] cell)  WHAT HAPPENS BETWEEN BINDING AND A RESPONSE? o Intracellular = communication between INTERNAL parts of the cell, signaling molecule-receptor binding initiates cascade of intracellular events leading to a response [AKA second messenger pathway/signal transduction pathway/intracellular pathway]  WHY A SIGNAL TRANDSUCTION PATHWAY INSTEAD OF DIRECT?  Signal transduction pathways amplify original signal (not 1:1)  Modulating the Response – Cross Talk  Signal transduction pathways provide many points where response can be regulated (activated/inhibited)  **Signaling molecule-receptor binding causes CONFORMATIONAL CHANGE of the receptor which initiates a signal transduction  Kinases = phosphorylate  Phosphatases = dephosphorylate  *Stimulate/inhibit pathway components by adding/removing phosphates  G Protein-Coupled Receptor (GPCR)  Integral receptor that’s associated with a signal transduction pathway  Signaling mlc binds to binding site, conformational change in receptor, cascade of events initiated by conformational change (GDP removed and GTP added  activated)  Cyclic AMP Signal Transduction Pathway nd  2 messenger cAMP (not protein)  Made from ATP conversion  catalyzed by Adenyl Cyclase  Protein Kinase A then phosphorylates CREB activating it [cellular response], CREB binds to transcription factor on DNA, initiates DNA transcription 1. Signaling mlc binds to receptor 2. Receptor conformational change (active form) activates G protein (GDP exchanged for GTP) 3. Activated G protein activates adenylyl cyclase 4. Adenylyl cyclase catalyzes conversion of ATP to cANP 5. Cyclic AMP binds to + activates protein kinase A 6. Activated protein kinase A phosphorylates other proteins in cell  response  Terminating the Response o Signaling mlc removed from receptor  receptor returns to inactive shape o G protein returns to inactive form (GDP bound) + returns to GPCR  deactivates adenylyl cyclase o cAMP converted to AMP by phophodisesterase (PDE) o Protein kinase A deactivated in absence of cAMP  Modulating the cAMP Pathway CHAPTER 9: CELL CYCLES  Cell Cycle = cycle of cell growth + division for the purpose of duplication  Cell Division = dividing of one cell into two (parent cell divides into 2 daughter cells  parent cell doesn’t exist after division) o Required for reproduction, growth/development/tissue renewal/repair o 2 Types of Cell Division  Mitosis (division of somatic cells) + Meiosis (division of germ cells)  Genetic Material (Heritable Information) o DNA located in nucleus, organized into chromosomes (made of chromatin = complex of DNA + associated w/protein) o DNA Organization in Eukaryotes  Histones pack eukaryotic DNA at successive levels of organization  Many non-histone proteins have key roles in the regulation of gene expression  chromosomal proteins of eukaryotes  DNA + associated protein complex = CHROMATIN  DNA wraps around a nucleosome (2 mlcs each of histones H2A, H2B, H3, H4), linker DNA connects adjacent nucleosomes, binding of histone H1 causes nucleosomes to package into a coiled structure (solenoid or 30nm chromatin fiber)  Euchromatin = loosely packed region, permits easy access to genes for RNA transcription (genes active)  Heterochromatin = densely packed masses, genes are inactive  ***both condense during nuclear division into thick, rodlike CHROMOSOMES o Chromosomes  All different, contain different genes, are different lengths  23 (HAPLOID) chromosomes in human cell, but 2 sets = 46 total (DIPLOID)  Individual chromosomes recognizable only during mitosis (when not dividing, chromosomes are thin + form a network in nucleus)  Daughter cells = identical copies of the parent cell (each daughter cell contains same DNA as parent cell did  DNA must be replicated)  DNA and Cell Division o **Number of different chromosomes doesn’t change following replication, only the amount of DNA does o DNA is thin + long, gets replicated, condenses into CHROMATID, cell divides + DNA returns to thin form  Always in pairs – SISTER CHROMATIDS = DNA replicates [replicated chromosome, contains same DNA], attached by proteins at CENTROMERE, KINETOCHORE proteins also associated w/this region  Cell Cycle o Interphase:  G1 Phase (first gap)  cell grows, produces more protein, organelles  S Phase (synthesis)  DNA replicated  G2 Phase (second gap)  cell grows further in preparation for division o Mitosis:  Division of one nucleus into 2 nuclei contain identical DNA  Parent nucleus dissolves + 2 new nuclei are formed following separation of DNA  DNA replicates + condenses into SISTER CHROMATIDS which line-up along midline, separate + move to opposite sides (by mitotic spindle), nuclear membrane forms around each chromosome (2 nuclei)  Mitotic Spindle  composed of microtubules, begins at centrosome, develops through prophase, prometaphase + metaphase, microtubules attach to kinetochore of each sister chromatid, motor proteins pull sister chromatids apart + move DNA replicates to opposite sides (anaphase) **once separated sister use term chromosome 1. Prophase  DNA replicates condense (fold/coil – short chubby appearance), chromosomes present as sister chromatids  Mitotic spindle begin to form as microtubules develop from centrosome  Centrosomes move to opposite poles (microtubules lengthen) 2. Prometaphase  Nuclear membrane breaks down  Kinetochore forms at centromere of sister chromatids  Mitotic spindle continues to form and centrosomes pushed towards poles  Some microtubules of mitotic spindle begin to attach to kinetochores 3. Metaphase  Sister chromatids line up at midline (metaphase plate) by microtubules  Mitotic spindle is complete  Centrosomes are at poles and microtubules at full length  Kinetochore protein of each sister chromatid attached to a microtubule 4. Anaphase  Proteins holding sister chromatids together cleaved by enzymes  Sister chromatids pulled apart + each chromosome is moved to opposite sides using motor proteins  Microtubules attached to sister chromatids reduce in length  Cell lengthens 5. Telophase  Complete set of chromosome located at opposite sides of the cell, become encapsulated by nuclear membrane (2 nuclei form)  Chromosomes begin to de-condense  Mitotic spindle completely reduces  Cytoplasm beings to divide 6. Cytokinesis  In animal cells  division of cytoplasm by contractile ring, muscular microfilaments (actin + myosin) located at contractile ring continually contract, which creates cleavage on extracellular surface  In plant cells  new cell plate formed at midline, separating cytoplasm  Cell Cycle Control System o 3 major checkpoints (G1, G2, M) o Checks: favourable environmental conditions, everything that should have occurred has occurred, no damaged components (eg. DNA) o “Go“ Signal  Cyclin-dependent kinases (cdks) regulate cell cycle (phosphorylate), other proteins (cyclins) also involved CHAPTER 15.4: THE LOSS OF REGULATORY CONTROLS IN CANCER  Problems w/cell cycle control system linked to abnormal cellular growth + cancer  Genes coding for proteins involved in cell division are called PROTO-ONCOGENES + can be altered to become ONCOGENES (promote uncontrolled cell growth + potential cancerous state)  Tumor-suppressor genes code for proteins that normally inhibit cell division can be altered  increased cell division instead (eg. Tp53)  Radiation/Chemotherapy target cell cycle of cancer cells to try to cease production of cancer cells, remaining parent cells eventually die  no production of daughter cells + cancer disappears (remission) CHAPTER 13: DNA REPLICATION  Semiconservative Model hypothesized by Watson + Crick  replicated DNA composed of parent (old) and daughter (new) strand of DNA  2 other models tested  conservative replication, dispersive replication  Involves over 12 enzymes, human DNA takes only a few hrs, bacteria < 1 hr  Origin of Replication o Begins here at specific nucleotide sequence, initiating proteins recognize the sequence o Bacteria singular, circular DNA) have 1 origin o Eukaryotes have 100s-1000s of origins  Replication Bubble + Replication Forks o DNA strands unwind + separate to form replication bubble o Replication occurs in BOTH directions (towards/away from replication forks) o Multiple origins + both directions = faster replication  DNA Replication o Helicases = enzymes that unwind + separate the DNA strands at replication forks o Single-Strand Binding Proteins = proteins that stabilize separated strands o Topoisomerase = relieves twisting pressure on still wound DNA ahead of replication fork, breaks/twists/rejoins DNA o Templates = each unwound “parent” strand serves as a template for a new complementary strand of DNA o RNA Primer = DNA nucleotides cannot be attached to template (must have starting point)  RNA primer from which the complementary DNA strand is built o DNA Polymerase = catalyze the addition of “new” nucleotides to “parent/template” strand starting at 3’ end of the RNA primer; complementary DNA created in 5’ – 3’ directions (DNA polymerase moves along “parent” DNA from 3’-5’) o Leading Strand = elongation from origin of replication towards replication fork, elongates continuously (RNA primer required only for initiation) o Lagging Strand = elongation away from replication fork, elongates in segments (Okazaki Fragments), each one primed separately  Primase adds the RNA primer
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