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CELL 120 Unit 3
Unit 3 Cell 120
| Question | Answer |
|---|---|
| Local signaling and the 3 methods | On site of the cell. Close proximity. 1. Direct contact 2. Cell junctions 3. Signaling molecules |
| Paracrine signaling | Releases signaling molecules to cells close by. Like Neurotransmitters in the synaptic gap for synaptic signaling |
| Long distance signaling | Hormones released in one part of the body sent through blood stream to another part of the body with specific receptors for that hormone. |
| The 3 stages of cell signaling | Signal reception, signal transduction, cellular response |
| Signal reception | Ligand (specific signal molecule). + and - interactions bond the ligand to the receptor. The start of the chain. |
| GCPR | G Protein Coupled Receptor. 7 Transmembrane. Water soluble ligands. Works with G proteins, activated by Guanine triphosphate (GTP). G protein bobs like a buoy to the enzyme. |
| Receptor tyrosine kinases | RTKs: Catalyze the phosphorylation (transfer phosphate from ATP to a protein). Can trigger multiple transduction pathways at once. Abnormal functions related to cancer. (Phosphate binds to tyrosine on RTK, activating other relay proteins) |
| Ligand gated ion channels | Passive diffusion of ions when the ligand binds to the receptor and opens the channel. Active transport is used to get that substance back out. |
| Intracellular receptor | In the cytoplasm or nucleus. Small non-polar molecules like hormones that diffuse through the membrane easily find these receptors, and it primarily leads to turning on/off specific genes. |
| Estrogen Receptor Signaling | Pregnancy, menopause, bone and heart function. Binds directly to DNA, changing gene expression. |
| Transduction pathway | Multi-step process. At each step, the signal is transduced into a different form, like changing the shape of a protein. |
| Phosphorylation Cascade | Protein Kinases in a chain of phosphorylation/dephosphorylation |
| Phosphorylation/dephosphorylation | Regulate protein activity by moving phosphates. |
| Protein Phosphatase | PP. Move the phosphate from the protein back to ATP/GTP. On/off switch, up/down switch. |
| Second messengers | Small, water soluble, non-protein molecules or ions. Spread by diffusion and participate in transduction pathways. |
| Cyclic AMP | cAMP is a 2nd messenger manufactured by adenylyl cyclase. |
| Adenylyl Cyclase | A membrane enzyme that converts ATP to cAMP in response to extracellular signals. Activates protein kinase A, which phosphorylates other proteins. Regulated by G proteins. |
| cAMP and Chorea | Chorea produces a toxin that keeps GCPRs in their active states, so it is continually making cAMP, which causes the intestines to produce a lot of salt. Loss of water and salt. |
| Calcium ions | 2nd messenger widely used. Outside concentration is high, so a small amount entering does a lot. Inositol triphosphate (IP3) and diacylglycerol (DAG) help raise calcium levels. |
| Cell Response | Some responses regulate activity, turn on/off genes to regulate enzymes, open/close channels, change metabolic pathways. |
| 4 aspects of signal regulation | 1. Amplification 2. Specificity 3. Efficiency 4. Termination |
| Amplification | At each step, the # of activated products is much greater than the preceding step. (1 epinephrine breaks down 100 million glucose) |
| Specificity | Different proteins detect different molecules and activate different pathways. "Cross talk," for the cell to coordinate activities. |
| 4 different paths of a transduction pathway | 1. Linear (straight) 2. Branched (1 receptor activates 2 paths) 3. Reinforced (2 receptors lead to 1 path) 4. Different receptor, but same ligand as above, but triggers a different resposne |
| Promiscuous ligands | Signal molecule that can trigger several different responses, like chloroquine as a medication for malaria, anti-cancer, immune... |
| Eiffecency | Scaffolding proteins and signal complexes attach relay proteins together for speed and efficiency. |
| Termination | Unbound receptors become inactive. No reason to keep working for no reason. |
| Apoptosis | Programmed cell death. Cell components packaged off into vesicles to be digested by scavenger cells. This prevents enzymes from leaking out and damaging neighboring cells. Triggered by DNA damage, protein misfolding. Inside/Outside signals. |
| How is apoptosis important for evolution? | The formation of the human hand. (Apoptosis occurs between fingers). |
| Mitosis | Parent cell --> 2 identical daughter cells. Interphase, mitosis (prophase, metaphase, anaphase, telophase), cytokinesis. |
| Roles of Cell division | Asexual reproduction of single cell organisms, embryonic development, and continual renewal of cells (especially RBCs) |
| Genome | All the DNA in a cell- Humans have 23 pairs of chromosomes, each containing thousands of genes. Sphagetti until cell division. |
| Chromatin | Made when: DNA condenses around the histone (spool protein). |
| Somatic cells | Most body cells. Skin, neurons, intestines... 2 sets of chromosomes. Undergoes mitosis |
| Gamates | 1/2 the chromosomes. Sperm and egg. Undergoes meiosis. |
| Sister Chromatids | 2 copies of a chromosome bound together: X |
| Interphase | Gap 1: growth, S phase: DNA copied, Gap 2: more growth and organelle replication. 90% of cell cycle |
| Prophase | Nuclear membrane and nucleolus disappear, chromatin --> chromosomes, the 2 centrosomes at opposite ends form mitotic spindle. |
| Metaphase | Nuclear envelope gone, Sister Chromatids align in the center of the cell, spindles extend out. |
| Anaphase | Separate chromatids (chromosomes) pulled to either side. Spindles press against the membrane to prepare to split. |
| Telophase | Complete sets of chromosomes reach spindles, nuclear envelope starts to form, and chromosomes go back to chromatin spaghetti. |
| Mitotic spindles | Microtubules that control cell movement, guide chromosomes. Come from centrosome. |
| An Aster | The radial array of microtubules |
| Kinetochore | Protein complex for each sister chromatid that helps with interactions between the spindle and the chromosome. |
| Seprase | In anaphase, the cohesions of the sister chromatids are dissolved at the center. ( X --> l l ) |
| Cytokenisis | Contractile ring of microfilaments forms around, called cleavage. Basically a belt that gets progressively tighter until the cell divides. |
| Binary Fission | Cytokinesis for bacteria (prokaryotes) No organization except for the DNA migrating to opposite ends, then the membrane pinches off. |
| What regulates the cell cycle? | Rate of cell division and apoptosis. Intrinsic and extrinsic factors. |
| Cell cycle check points | G1 check: makes sure all pieces in place G2 check: Makes sure centromeres are ready and that DNA was synthesized correctly. M check: All aligned in metaphase |
| Cyclin and Cyclin dependent Kinases | The CDK's activity rises and falls with the fluctuating concentration of cyclin. Cyclin binds to kinase which phosphorylates substrates, which is what gets the cell through the check point. |
| Growth Factors | Ligand that binds to RTK. Dimerizes, the kinases phosphorylate each other and it starts the cascade, activating CDKs |
| Density dependent inhibition | Once cells touch they stop replicating |
| Anchorage dependance | Cells don't divide unless adhered to something. |
| How cancer cells override everything | They don't stop when the growth factor is gone, they make their own, use other cells, or send the signal without one. |
| Transformation | When a cell goes cancerous: Just doesn't stop. Gas pedal to the floor and the break line cut. |
| Anti-Cancer therapies | Target the cell cycle. Inhibit microtubule spindles, prevent S-phase. |
| Main function of mieosis | Result in 1/2 copies of chromosomes in sperm and egg cells. Diploid--> 4 unidentical haploid daughter cells. |
| Inheritance/Heredity | Passing traits from one generation to another. |
| Genetics | The study of inherited variation |
| Genes | Made of segments of DNA. Genes code proteins: determine shape, which determines structure, and thus expression of physical traits. Passed on by gametes. |
| Locus | The specific location of a gene-- always in the same place on a chromosome, but the gene itself has variations. |
| Karyotype | Ordered display of chromosomes, 1-23 (Biggest to smallest autosomes, then the sex chromosomes) |
| Homologous chromosomes | A maternal and paternal chromosome. Base pairs of each very, but they have similar structures, same length, centromere placement, staining pattern, and control the same characters. |
| Sex chromosomes | The female XX and male XY |
| Diploid cell | 2 sets of chromosomes. It is the full compliment: 2n=46 (n=23) |
| Zygote | A fertilized egg, 2 haploid cells unite to create 1 full set of chromosomes from each parent. Then it produces somatic cells by mitosis. |
| What produces haploid gamates in humans | Testes and ovaries |
| Prophase I | Crossing over of genes occurs in chiasmata |
| Metaphase I | Homologs line up at metaphase plate, attached to the kinetochore, and the microtubules start to pull. |
| Anaphase I | The cross over is visible. Sister chromatids remain as one towards the poles. |
| Telophase I | Each side of the cell has a haploid set up duplicated chromosomes. (There is no full compliment. The maternal and paternal sister chromatids are not together) |
| Meiosis II | CLOSEST TO MIEOSIS! No chromosome replication, no crossing over. The sister chromatids separate. Basically mitosis, it just results in haploid daughters. |
| What forms to separate cells in cytokenisis | Cleavage furrow in animals, cell plate in plants. |
| Spermatogenesis | Meiosis for sperm cells. Diploid germ cell --> 4 unidentical sperm cells |
| Oogenesis | Meiosis for egg cells. Diploid germ cell --> secondary egg cell + polar body --> Ovum + 3 polar bodies (super loads ovum with nutrients, organelles, mitochondria. Polar bodies only have DNA and will die) |
| Non-Sister chromatid crossing over | Break at specific points on each chromosome. Synaptonemal complex holds homologs close together. Synapsis repairs these DNA breaks, and matches it up with the corresponding segments from another non sister chromatid. |
| The 3 events that make meiosis unique | All in meiosis I 1. Synapsis and crossing over in prophase I 2. Aligned homologs at metaphase plate (sister chromatids not separating until anaphase II) 3. Cohesions don't cleave (unravel) until anaphase II |
| Translocation | A mismatch on homologs gone awry. One chromosome missing a segment, the other has double... Can code a new gene. |
| Non-disjunction | Gametes with too many or too few chromosomes. Separase doesn't work. |
| Disorders from non-disjunction | Kleinfelter syndrome: XXY or XXXY Turner syndrome: X0 Trisomies. |
| Ploidy | Haploid, diploid, just the number of SETS of chromosomes. |
| Model organisms | Drosophila melanogaster (fruit fly), worm, mouse, weed, yeast, fish. -Produce many offspring -Generation bred every 2 weeks -Only 4 pairs of chromosomes |
| Phenotype | Physical trait. Passed down through chromosomal theory. |
| Allele | Variation of a gene. You either have it, or you don't. Red eye fly or white eye fly. |
| Variations in sex chromosomes in other organisms (3) | Grasshoppers: f (XX) m (X) Chickens: 78 chromosomes. f (ZW) m (ZZ) Honey bee: f (32 diploid) m (16 haploid) |
| What are genes on the Y chromosome called? | SRY- sex determining region on Y. Responsible for development of testes and embryo. |
| Sex linked genes | Genes on X (1100 genes) and Y (78 genes). X linked have many functions and general genes. Y has sex determination genes. |
| X linked recessive genes to be inherited (what alleles do the maternal and paternal chromosomes need to have?) | Female needs 2 copies of allele (Rr or rr) and the male only needs one copy (R or r). See notes. |
| What are some X linked conditions? (3) | Color blindness, muscular dystrophy, hemophilia. |
| X inactivation | XX is toxic, so in embryonic development, one of the X's is randomly turned off by condensing so tight it can't be used: BARR BODY!! (If heterozygous in a gene Rr, activated X's evenly spread out) |
| XIST | X inactive specific transcript. A gene on the X chromosome that codes RNA to cover it so nothing can interact with it. |
| Disorders caused by structurally altered chromosomes (2) | Cri du chat- deletion of 5. Translocations of genes can also cause cancers. |
| Exceptions to Mendelian Inheritance | 1 in nucleus, 1 in mitochondria. |
| Genomic imprinting | Silencing certain genes, either the maternal or paternal. Mom's hair dad's eyes. |
| Extranuclear genes | Cytoplasmic genes, passed on by mother. DNA for organelles. Defects in mitochondrial genes --> not enough ATP produced. Nervous and muscular disorders. If known defects, can use donor egg w/mom's chromosomes. |
| The history of discovering DNA structure | Maurice Wilkins and Rosalind Franklin used x-ray crystallography to discover the sugar-phosphate backbone. James Watson and Crick then deduced the antiparallel double helix structure with purines to pyrimidines. |
| Origins of Replication | The bubbles |
| Helicase | Untwist at replication fork (the unzipping mechanism) |
| Single Strand Binding Proteins | Stabilize single strand DNA by binding to it. |
| Topoisomerase | Relief by breaking, swiveling, and rejoining DNA |
| DNA Polymerase I and III | 20 nucleotides per second, 5' to 3'. 20 nucleotides p/s in humans, 500 in bacteria. Lays down in pairs with dehydration reactions, always moving towards the helicase at the replication fork. 1 replaces the RNA on the lagging, 3 is for the leading strand. |
| Primase | Synthesizes RNA primer |
| RNA Primer | Recruits DNA Polymerase to start laying down nucleotides. |
| Replication of the lagging strand | Done in segments: Okazaki fragments. Hit primer, polymerase I hits something, stops, then starts once more RNA primer added. |
| Ligase | Smooths over DNA segments in lagging strand. |
| The DNA Replication Complex | Polymerase I and III Helicase Primase -- RNA Primer Topoisomerase Single Strand Binding Proteins |
| How can DNA be damaged? | Smoke, chemicals, x-rays, and spontaneous changes. |
| Nuclease | Enzyme that performs nucleotide excision repair: cuts off damage, polymerase lays down new, and ligase smooths + glues. |
| How mutations arise | There is 1 error per genome, 3,000 errors per replication of DNA. If these changes become permanent, they can be passed down, and natural selection takes care of the rest. |
| Telomere replication | Ends of chromosomes: telomere gets shortened through replication, so telomerase extends the end so that that genetic info isn't lost. Reaching the telomere tells the DNA it can't replicate more, limiting cell division! Only time primase goes 3' --> 5' |
| Telomeres and aging | We lose base pairs as we age. No telomere, no replication. Thus, aging. Long telomere --> look young, but more likely to get cancer because the telomere is what stops DNA replication. |
| DNA in bactera | Circular, double stranded, found in nucleoid. |
| DNA structure in eukaryotes | Linear double stranded helix. Packaged as CHROMATIN, DNA wound tightly around histones. |
| Nucleosome | DNA wrapped 2 times around an octane histone core. These histones have amino acid tails that help regulate gene expression. |
| Acetylation | Acetyl group added to the histone tail. Acetyl group is negative. Because the sugar-phosphate backbone is negatively charged, they repel --> LOOSER PACKED EUCHROMATIN |
| Methylation | Methyl group added, which is positive, so the DNA backbone and methyl group attract, making the DNA pack tighter around the histone --> HETEROCHROMATIN (harder to express genetic info) |
| Gene Expression | Translating DNA code into proteins by transcription and translation. |
| Central Dogma of gene expression | Cells have a chain of command from DNA to RNA to protein |
| Primary transcript | Initial RNA transcript from a gene |
| Codon | Triplets that make up genetic code. Like AUG, AAA, etc. All proteins start with the methionine, coded by AUG. |
| Template Strand | This strand of DNA is like a mold that is filled with plaster (the RNA) so that the end result looks like the statue. Using the inverse. It is always the same strand for the same gene. (The other strand would give you different amino acids) |
| Reading frame | Groupings of codons. Like making sure its AAG UGU CGA instead of A AGU GUC GA... |
| RNA Polymerase | Pries open the 2 DNA Strands and lays down new nucleotides complementing the template and attaches them to each other. No primer needed. |
| Promoters | DNA sequence where RNA polymerase attaches, unique to each gene. |
| Terminator | Sequence for the end of RNA transcription in BACTERIA |
| Transcription unit | Stretch of DNA transcribed |
| Synthesis of RNA Transcript in Transcription part of gene expression | Initiation, elongation, termination |
| Transcription Factors | Guide the binding of RNA polymerase by opening chromatin. |
| Transcription initiation complex | Transcription factors, RNA Polymerase bound to promoter. |
| TATA box | Part of a promoter Thymine Adenine TATA recruits RNA polymerase, which once bound, starts transcription at AUG! |
| Initiation | Transcription factors bind to DNA and the Transcription initiation complex forms when the RNA polymerase is recruited. |
| Elongation | Unwinds 10-20 nucleotides at a time. It is an endergonic reaction powered by breaking a phosphate. Add nucleotides to 3' end. |
| Termination | Poly A Site of 10-35 nucleotides the polyadenylation sequence to protect the RNA transcription (string of AAAA...) |
| Intron | Non-coding segment of RNA. Sometimes regulate gene expression, sometimes they can become RIBOZYMES by folding on themselves. (These help with splicing) |
| Exon | Expressed region that is later translated into amino acid sequence. |
| Spliceosome | RNA and prottien combo that recognize where things need to be removed, so it removes the introns. |
| Alternative RNA splicing | Splicing exons in different ways. Some might be cut out. So, many different protein combinations are possible. A way to enhance the complexity of how many proteins you can make while keeping less genes. |
| Evolutionary importance of alternative RNA splicing | Corn doesn't use splicing! Hence why it has 32,000 genes and we have 20,000 genes: we can DO MORE with those genes |
| Protein domains | Regions of a protein. Each region is coded by an exon, so if the exons shuffle, you get a new protein. |
| Transfer RNA (tRNA) function | 64 tRNAs (1 per nucleotide triplet combo). Non-coding. Transfer amino acids to the growing polypeptide (translating from nucleotide to peptide) . |
| tRNA structure | L shape, with anticodon on one end (base pairs with complementary codon on mRNA), and the corresponding amino acid on the 3' end. |
| Aminoacyl-tRNA synthetase | Enzyme that matches tRNA to amino acid. |
| Function of ribosomes | Sites of translation. Match tRNA anti-codons to mRNA codons. |
| Ribosomal binding sites and functions | A- holds the next tRNA in line P-holds the tRNA that carries the amino acid chain (peptide synthesized w/ dehydration reaction) E- exit site. Discharges tRNAs. |
| Translation | Final RNA transcript --> polypeptide chain. Initiation, elongation, termination. |
| Initiation | Small ribosomal subunit binds with mRNA and the tRNA initiator. Subunit moves until it hits start codon on mRNA. Initiation factor proteins bring in large ribosomal subunit (APE sites), completing the translation initiation complex. |
| tRNA initiator | UAC anti-codon to match with AUG, carries methionine |
| Elongation | Amino acids added 5' to 3' to C terminus end with the help of elongation factors. 1. Codon recognition 2. Peptide bond formation 3. Translocation. Energy in 1+3. Moves codon by codon, empty tRNA exits to reload in cytoplasm. |
| Termination | A site hits the stop codon and accepts the release factor protein which adds H2O instead of an amino acid (hydrolysis). This releases the polypeptide, and the translation assembly falls a part. |
| Point mutations | 1 nucleotide changes. (Sickle cell disease) There are 2 types: Single nucleotide-pair substitutions, and nucleotide-pair insertions/deletions |
| Mutations | Changes in the genetic information of a cell |
| Types of substitution mutations | Point: nucleotide pair substitutions Silent: Different base pair codes for same amino acid, no effect. Missense: code for incorrect amino acid Nonsense: Sequence changes to stop codon. |
| Insertions and deletions | Add or lose nucleotide --> frameshift mutation that changes the entire protein. |
| Mutagen | Physical/chemical agents that change DNA. Called a carcinogen if it causes cancer. |
| CRISPR-Cas 9 | Cas-9 enzyme cuts double stranded DNA, triggering the DNA repair system, and the CRISPR replaces the bad section that was cut out to prevent frame-shift mutations and fix the gene. |
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lilelise
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