Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings PowerPoint Lectures for Biology, Seventh Edition Neil Campbell and Jane Reece Lectures by Chris Romero Chapter 16 The Molecular Basis of Inheritance

Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings

LE 16-2 Living S cells (control) Living R cells (control) Heat-killed S cells (control) Mixture of heat-killed S cells and living R cells Mouse dies Living S cells are found in blood sample Mouse healthy Mouse dies RESULTS

LE 16-3 Bacterial cell Phage head Tail Tail fiber DNA 100 nm

LE 16-6 Franklin’s X-ray diffraction photograph of DNA Rosalind Franklin

LE end 3 end 5 end 3 end Space-filling modelPartial chemical structure Hydrogen bond Key features of DNA structure 0.34 nm 3.4 nm 1 nm

LE 16-UN298 Purine + purine: too wide Pyrimidine + pyrimidine: too narrow Purine + pyrimidine: width consistent with X-ray data

LE 16-9_4 The parent molecule has two complementary strands of DNA. Each base is paired by hydrogen bonding with its specific partner, A with T and G with C. The first step in replication is separation of the two DNA strands. Each parental strand now serves as a template that determines the order of nucleotides along a new, complementary strand. The nucleotides are connected to form the sugar-phosphate back- bones of the new strands. Each “daughter” DNA molecule consists of one parental strand and one new strand.

In Prokaryotes – 1 bubble of origin, In eukaryotes, many at once!! In eukaryotes, DNA replication begins at may sites along the giant DNA molecule of each chromosome. Two daughter DNA molecules Parental (template) strand Daughter (new) strand 0.25 µm Replication fork Origin of replication Bubble In this micrograph, three replication bubbles are visible along the DNA of a cultured Chinese hamster cell (TEM).

Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Antiparallel Elongation The antiparallel structure of the double helix (two strands oriented in opposite directions) affects replication DNA polymerases add nucleotides only to the free 3  end of a growing strand; therefore, a new DNA strand can elongate only in the 5  to  3  direction. Nucleotides in DNA backbone are bonded from phosphate to sugar between 3 & 5 carbons – DNA molecule has “direction” – complementary strand runs in opposite direction

LE Parental DNA 5 3 Leading strand Okazaki fragments Lagging strand DNA pol III Template strand Leading strand Lagging strand DNA ligase Template strand Overall direction of replication

Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Proofreading and Repairing DNA DNA polymerases proofread newly made DNA, replacing any incorrect nucleotides that they catch! In mismatch repair of DNA, different repair enzymes correct errors in base pairing after synthesis. In nucleotide excision repair, enzymes cut out and replace damaged stretches of DNA. Humans have 130 different enzymes to this but errors still get through (1/100,000 base paris).

Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings What if these enzymes get mutated??? Bad results.. Xeroderma pigmentosum, or XP, is an autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient. In extreme cases, all exposure to sunlight must be forbidden, no matter how small or cancer will occur. autosomal recessivegenetic disorderDNA repairultraviolet

Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Eukaryotic chromosomal DNA molecules have at their ends nucleotide sequences called telomeres (not prokaryotes) Telomeres are PROTECTIVE ends (sequence TTAGGG)– they do not prevent the shortening of DNA molecules, but they do postpone the erosion of genes near the ends of DNA molecules. As you age – the telomeres erode, you age and die. The telomere shortening mechanism normally limits cells to a fixed number of divisions, and animal studies suggest that this is responsible for aging on the cellular level and sets a limit on lifespans..

Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings If chromosomes of germ cells became shorter in every cell cycle, essential genes would eventually be missing from the gametes they produce (so…deformed offspring?) An enzyme called telomerase catalyzes the lengthening of telomeres in sex cells only. Could we apply this to all cells??