EXAM 1 - Population, DNA Replication, Mitosis Meiosis

Nitrogenous base pentose sugar phosphate double helix 5’-3’ antiparallel structure

Two coils of DNA on Histone core ~ 200 base pairs of DNA Octomere on each of H2A, H2B, H3, H4 H1 - space between nucleosome

• Primar struc. - 2 coils of DNA on nucleosomes core • Secondary struc. - helical array of nucleosomes • Tertiary - Packing of nucleosome arrays into chromatin visible chromosomes are transcriptionally inert - so raveled up can’t unravel and make gene copies

*Heterochromatin: densely packed, not transcribed (some nonsense, some repressed) - Constitutive: repeated sequences, genes not expressed - Facultative: the form of an entire chromosome that is expressed - ex> — x chromosome barr body: color blind (can’t see red or yellow well), hemophilia (unable to clot blood) *Euchromatin: active genes, transcribed as needed - found on nucleosomes core and area between

small, densely staining structure in the cell nuclei of female mammals - condensed in X chromosome ex. color blind, hemphilia

Cyclins activate Mitotic cdks (cyclin dependent protein kinases)

Cyclins activate Mitotic cdks (cyclin dependent protein kinases) Protein kinases phosphorylate proteins (enzymes) to catalyze cell reactions When cyclins are added, cells move through cell cycle checkpoints

Cyclins activate Mitotic cdks (cyclin dependent protein kinases) Protein kinases phosphorylate proteins (enzymes) to catalyze cell reactions When cyclins are added, cells move through cell cycle checkpoints - found at 3 major checkpoints (G1, G2, M Phase)

Go (nondividing): muscle and nerves Cells that barely divide but can when stimulated: Liver (G2) Cells that rapidly divide: - Skin, hair - GI epithelium - Bone marrow, blood - Reproductive cells

p = protein 53 = 53 kilodaltons - Regulates cell division, wild type form halts cell divisions, arrests cells in G1 - mutant forms cause abnormal cell division - half of all cancers involve mutation of this gene - gene can trigger “apoptosis” – programmed cell death - some carcinogens are found to alter p53

• Oncogenic factors • Bcl 1 and 2 genes (B cell lymphoma) • BRCA 1 and 2: linked to 80% chance of breast, ovarian cancer • Ras gene • Cyclin proteins (may be triggered by bcl gene)

• P53 gene • bax genes • ICE (interleukin converting enzyme) • Ubiquitin • these same factors can also trigger apotosis

• P53 gene • bax genes • ICE (interleukin converting enzyme) • Ubiquitin • these same factors can also trigger apoptosis

Initiator Proteins: unwind DNA double helix Helicase: continues winding Topoisomerase: swivel prevents tangling of DNA supercoils

DNA polymerase directs DNA replication DNA replicates in a 5’ to 3’ direction Begins w/ attachment of RNA primer followed by DNA polymerase Where possible, RNA primer replaced via exonuclease/ ligase

Initiator Protein Helicase Topoisomerase Exonucleases Endonucleases RNA Primer DNA Ligases DNA Polymerase Leading Strand Lagging Strand

Unwind DNA - binds to origin of replication an initiate unwinding of DNA double helix - both cell types

Unwinds dsDNA - both cells (eukary and prokary)

Sins the ends of the DNA so the stands won’t get knotted up

an enzyme which removes successive nucleotides from the end of a polynucleotide molecule

an enzyme which cleaves a polynucleotide chain by separating nucleotides other than the two end ones

DNA synthesis 1. Leading Strand: s looking greek symb. - eu - 2. Lagging Strand - alpha - eu -

(both cell types) – makes covalent bonds to join together adjacent DNA strands, including the Okazaki fragments in lagging-strand DNA synthesis and the new and old DNA segments in excision repair of DNA