Genetics Notes week 7
Genetics Notes week 7
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This 3 page Reader was uploaded by Becca Sehnert on Tuesday March 1, 2016. The Reader belongs to a course at a university taught by a professor in Fall. Since its upload, it has received 26 views.
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Date Created: 03/01/16
WEEK 7 NOTES MONDAY Spontaneous mutations arise from replication errors and DNA damage • Replication errors o DNA polymerase occasionally inserts incorrect nucleotides Tautomeric shifts • Thymine (keto) H bond with Adenine (amino) • Thymine (enol) has anomalous base-pairing arrangements and H bonds with Guanine (keto) • Depurination and deamination are most common causes of spontaneous mutation • DNA may also suffer oxidative damage as a by-product of normal cellular processes o Adenine can have Nitrogen base leave and make a hypoxanthine that pairs with cytosine Induced mutations • Experimental changing of DNA caused by chemicals and radiation Deamination can lead to what type of mutation? a. Transition b. Substitution c. Missense of nonsense mutation d. All of the above e. None of the above LOOK AT SLIDES FOR PICTURES OF TYPES OF MUTATIONS Alkylating agents donate alkyl group Intercalating agents • Acridine dydes cause frameshift mutations by intercalcating between base pairs • Small part of DNA unwinds and causes frameshift mutation UV light is a mutagen • Shift in pi bonds and get distorted a bit • Thimine dimers –stalls polymerase Radiation • Ionizing radiation in form of x rays, gamma rays, and cosmic rays are mutagenic • Hydroxyl reacts with DNA and causes proglems Mutations in humans • Muscular dystrophy –mutation in gene dystrophin • More severe (DMD) result of frameshift mutation in dystophin gene o Leads to nonfunctional truncated protein o Sometimes worse being there than not at all • Less severe (BMD) due to alteration of protein by missense mutations Which of following categories of mutations are not possible to pass to offspring? a. Silent b. Somatic c. Frameshift d. Induced e. Autosomal Repair • DNA polymerases able to recognize and correct errors in replication = proofreading • Other mechanisms exist • Depend on type of damage o One strand of DNA § Incorrect base, mismatch –identify incorrect base, remove, and resynthesize (they know which is old and new strand) § Damaged base –enzymatically reverse damage, remove damaged base then sugar and phosphate and resynthesize, or remove region of damage and resynthesize o Broken DNA (double-strand break) § Relegate (sometimes problems with this but at leads you have DNA) § Replace by copying another molecule (homolog or sister as template) • Mismatch pair o Correct errors that remain after proofreading o Mismatched base recognized and removed o Recognizing “correct” base is important and depends on man features, including methylation • Postreplication repair o When DNA replication skips over lesion, homologous recombination can repair the strands • SOS repair o Allows DNA synthesis to become error-prone o Completely stalling and cant move on at all o Hands off replication to less accurate replicators o These are just to replicate through DNA errors that cant normally be replicated with good replicators just to put SOMETHING there o SOS repair is mutagenic and allow cell to survive DNA damage that might otherwise kill it • Photoreactivation o Removes thymine dimers caused by UV light o Process depends on protein called photoreactivation enzyme (PRE) o Blue light photons are used as energy source o Doesn’t operate in mammals • Base excision repair (BER) involves LOOK AT SLIDES o Recognize damaged base by DNA glycosylase o Cut off • Nucleotide excision repair (NER) repairs bulky lesions and involves uvr genes o This is how mammals repair the dimers o Phosphosdiester bond broken and several nucleotides removed WEDNESDAY
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