Chapter 16: DNA and Protein Complex PDF

a DNA and protein complex found in eukaryotic cells' nucleus chr...

a DNA and protein complex found in eukaryotic cells' nucleus chromosomes fit into nucleus through multilevel packing system it undergoes changes during cell cycle less condensed euchromatin loosely packed types high condensed heterochromatin chromoatin tightly packed chromatin organizes into a 10-nm fiber, while most is compacted into a 30-nm fiber chromosomes occupy restricted nucleus regions despite not being highly condensed most chromatin is loosely packed and condenses before mitosis interphase chromosomes chromatin regions (centromeres and telomeres) into heterochromatin dense heterochromatin packing hinders cell expression of genetic information histones can undergo chemical modifications affecting chromatin organization genes found on chromosomes double-stranded circular DNA molecule associated with small amount of protein DNA and protein components become genetic material bacterial chromosome Morgan's group selection of appropriate experimental organisms crucial DNA is supercoiled and found in nucleoid difference between DNA's role in heredity discovered through bacteria and viruses linear DNA molecules associated with large amount of protein eukaryotic chromosomes he studied genetic role of DNA limitations of DNA polymerase cause issues with linear DNA of eukaryotic chromosomes pathogenic replication machinery doesn’t complete 5' ends, so repeated rounds of replication produce shorter DNA molecules with uneven ends worked with strains of bacterium prokaryotes have circular chromosomes, avoiding this issue harmless DNA molecules have special nucleotide sequences at their ends he mixed heat-killed remains of pathogenic strain with living cells of harmless strain, led to transformation to became pathogenic transformation change in genotype and phenotype due to assimilation of foreign DNA happened in eukaryotic chromosomal living R bacteria had been transformed into pathogenic S bacteria don’t prevent shortening of DNA molecules Griffith concluded from dead S cells that allowed R cells to make capsules do postpone erosion of genes near ends of DNA molecules telomeres shortening of telomeres linked to aging shortening of germ cell chromosomes could lead to essential gene loss in gametes telomeres may protect cells from cancer by limiting cell divisions relationship with cancer replicating ends of DNA molecules evidence of telomerase activity in cancer cells suggests cell persistence enzyme catalyzes lengthening of telomeres in germ cells telomerase they announced transforming substance was DNA Avery, McCarty, MacLeod concluded only DNA worked in transforming harmless bacteria into pathogenic bacteria also known as phages bacteriophages are viruses that specifically infect bacteria performed experiments showing DNA is genetic material of T2’s phage only DNA or protein of T2 enters E. coli cell during infection phage DNA entered bacterial cells, but phage proteins did not concluded Hershey, Chase DNA, not proteins functions as genetic material of phage T2 DNA polymerases proofread new DNA, replacing incorrect nucleotides repair enzymes correct errors in base pairing mismatch repair cigarette smoke ex. harmful chemical agents X-rays ex. harmful physical agents DNA can be damaged by undergo spontaneous changes nuclease cuts out and replaces damaged stretches of DNA nucleotide excision repair using X-ray crystallography to study molecular structure low error rate after proofreading repair produced picture of DNA molecule sequence changes can become permanent and pass to next generation evolutionary significance of altered DNA nucleotides proofreading and repairing DNA two outer sugar-phosphate backbones concluded mutations source genetic variation for natural selection nitrogenous bases paired in molecule's interior Wilkins, Franklin introduced double-helical model for DNA structure DNA, substance of inheritance, celebrated molecule hereditary information encoded in DNA, reproduced in all cells DNA program directs development of biochemical, anatomical, physiological, and behavioral traits DNA was helical Franklin's X-ray image enabled to deduce width of helix spacing of nitrogenous bases may be stationary during replication process DNA replication machine proteins participate in DNA replication form large complex photo pattern suggested DNA molecule was made up of two strands as double helix "reel in" parental DNA conformed to X-rays and DNA chemistry recent studies support model where DNA polymerase molecules double helix’s model "extrude" newly made daughter DNA molecules showed antiparallel backbones same base pairings didn't result in uniform width DNA replication complex The Molecular Basis of Inheritance Watson, Crick adenine (A) with thymine (T) they found specific base pairings guanine (G) with cytosine (C) explained Chargaff's rules: A = T, G = C suggested a possible copying mechanism for genetic material antiparallel structure of double helix affects replication each strand of DNA acts as template for building new strand in replication DNA polymerases add nucleotides only to free 3' end of growing strand semiconservative model of replication predicts each daughter molecule will have one old strand and one newly made strand new DNA strand can elongate only in 5' to 3' direction conservative model two parent strands rejoin along one template strand of DNA polymerase synthesizes competing models included leading strand dispersive model each strand is mix of old and new moving toward replication fork their experiments supported semiconservative model labeled old strand nucleotides with heavy nitrogen isotope labeled new nucleotides with lighter nitrogen isotope to elongate other new strand lagging strand first replication produced hybrid DNA, eliminating conservative model DNA polymerase work in direction away from replication fork second replication produced light and hybrid DNA, supporting semiconservative model Meselson, Stahl antiparallel elongation DNA replication short segments of DNA produced by discontinuous replication of lagging strand okazaki fragments is replication begins at particular sites enzyme joined between Okazaki fragment and RNA primer DNA ligase origins of replication where two DNA strands are separated opening up replication “bubble” a Y-shaped region where new DNA strands are elongating replication fork at end of each replication bubble helicases are enzymes that untwist double helix at replication forks single-strand binding proteins bind to and stabilize single-stranded DNA enzymes catalyze elongation of new DNA at replication fork getting started breaking primer require DNA polymerases topoisomerase corrects ahead of replication forks by swiveling DNA template strand rejoining DNA strands cannot initiate synthesis of polynucleotide feature initial nucleotide strand is short RNA they can only add nucleotides to 3’ end primer short (5-10 nucleotides long) 500 nucleotides per second in bacteria feature rate of elongation is about 3' end serves as starting point for new DNA strand 50 per second in human cells enzyme can start RNA chain from scratch each nucleotide added to growing DNA strand is nucleoside triphosphate primase adds RNA nucleotides one at time is nucleotide that supplies adenine for DNA synthesis during replication using parental DNA as template deoxyribose sugar dATP synthesizing new DNA strand each monomer loses two phosphate groups as it joins DNA strand difference between is primarily involved in energy metabolism ATP ribose sugar