NER in E. coli continued

فهرست عناوین اصلی در این پاورپوینت

فهرست عناوین اصلی در این پاورپوینت

● Lecture 10
● Types of mutations
● Substitutions that occur in protein-coding sequences
● EXAMPLES – substitutions
● Frameshift example
● SNPs
● SNPs can have variable effects
● Fate of DNA damage
● Examples of mutation fixation
● Human Genome
● Mutation Rate per bp
● Mutation rate per gene
● DNA mismatch repair
● MMR cont
● Uracil DNA glycosylase and BER
● Environmental DNA damage
● The discovery of NER
● The process of uvrABC excision of DNA damage is called nucleotide excision repair.
● NER in E. coli continued
● NER in mammalian cells
● There are 8 XP complementation groups
● XB Genes continued
● Some XP proteins are
● Cleaver’s study: Complementation groups of XP
● Developing an in vitro DNA repair system
● The in vitro assay
● How the incision product is detected
● Global Genomic Repair
● There are endogenous and exogenous sources of mutagens
● What do mutagens do?
● Types of Mutagens
● Alkylating agents
● Reactive sites on nucleotides
● Alkylating agents
● Mutagens don’t always start out that way
● Cytochrome P450 monooxygenase system
● General reaction
● Aflatoxin reaction
● EMS modification of DNA
● P450s are found in all cells but mostly in liver and small intestine
● P450 at work
● Endogenous DNA damage
● Deamination of Cytosine
● Sources of exogenous DNA damage
● UV Radiation,
Pyrimidine dimers
● How does DNA
damage cause mutations?
● See the man pat the pet cat
● Examples of repair mech’s
● DNA polymerases
● Nucleotide Excision Repair
● DNA Repair part 2
● Types of UV damage
● Nucleotide Excision Repair
● How UVDE works
● Mismatch repair
● DNA repair diseases
● Xeroderma Pigmentosum
● DNA repair diseases

نوع زبان: انگلیسی حجم: 3.36 مگا بایت
نوع فایل: اسلاید پاورپوینت تعداد اسلایدها: 84 صفحه
سطح مطلب: نامشخص پسوند فایل: ppt
گروه موضوعی: زمان استخراج مطلب: 2019/06/07 11:33:52

لینک دانلود رایگان لینک دانلود کمکی

اسلایدهای پاورپوینت مرتبط در پایین صفحه

عبارات مهم استفاده شده در این مطلب

عبارات مهم استفاده شده در این مطلب

‘, ., dna, ۳, ۵, mutation, cell, xp, damage, snp, repair, complex,

توجه: این مطلب در تاریخ 2019/06/07 11:33:52 به صورت خودکار از فضای وب آشکار توسط موتور جستجوی پاورپوینت جمع آوری شده است و در صورت اعلام عدم رضایت تهیه کننده ی آن، طبق قوانین سایت از روی وب گاه حذف خواهد شد. این مطلب از وب سایت زیر استخراج شده است و مسئولیت انتشار آن با منبع اصلی است.

در صورتی که محتوای فایل ارائه شده با عنوان مطلب سازگار نبود یا مطلب مذکور خلاف قوانین کشور بود لطفا در بخش دیدگاه (در پایین صفحه) به ما اطلاع دهید تا بعد از بررسی در کوتاه ترین زمان نسبت به حدف با اصلاح آن اقدام نماییم. جهت جستجوی پاورپوینت های بیشتر بر روی اینجا کلیک کنید.

عبارات پرتکرار و مهم در این اسلاید عبارتند از: ‘, ., dna, ۳, ۵, mutation, cell, xp, damage, snp, repair, complex,

مشاهده محتوای متنیِ این اسلاید ppt

مشاهده محتوای متنیِ این اسلاید ppt

lecture ۱ dna repair continued types of mutations deletions a part of the dna is missing anywhere from ۱ base pair to parts of chromosomes. insertions of new dna again ranging from ۱ to many base pairs point mutations a change in the nucleotide. two types transitions purine to other purine or pyrimidine to other pyrimidine. transversions purine to pyrimidine or pyrimidine to purine. ۵’ gaattc ۳’ ۳’ cttaag ۵’ substitutions ۵’ gatttc ۳’ ۳’ ctaaag ۵’ ۵’ gagttc ۳’ ۳’ ctcaag ۵’ deletion ۵’ gaatc ۳’ ۳’ cttag ۵’ ۱۹۹۹ lee bardwell ۵’ gaattc ۳’ ۳’ cttaag ۵’ insertion ۵’ gaacttc ۳’ ۳’ cttgaag ۵’ duplication ۵’ gaatattc ۳’ ۳’ cttataag ۵’ ۲ lee bardwell substitutions that occur in protein coding sequences silent changes a codon but not the encoded amino acid residue possible because the code is degenerate missense changes the encoded residue nonsense an amino acid encoding codon becomes a stop codon ۱۹۹۹ lee bardwell examples substitutions silent tgt cys tgc cys gca ala gcn ala n any missense tgt cys tgg trp nonsense tgt cys tga stop ۲ lee bardwell frameshift example nh۲ met thr leu lys cooh ۵’ atg acc ttg aaa taa ۳’ nh۲ met pro cooh ۵’ atg cct tga aat aa ۳’ delete a ۲ lee bardwell snps snps snps snps snps can have variable effects snps can have no effect. their change can be neutral to the protein e.g. a silent mutation. snps can have a subtle effect e.g lys to arg both are polar basic . this is what we suspect is happening in complex genetic diseases snps can have measurable effects a pronounced reduction in activity . snps can change protein function. a new substrate might be recognized. snps can complete eliminate the proteins ability to function. fate of dna damage tolerated ignored repaired can kill the cell or cause the cell to kill itself can become fixed resulting in a mutation note fixed repaired examples of mutation fixation replication of an unrepaired misincorporation replication of an unrepaired cytosine deamination deaminated cytosine uracil human genome haploid size ۳۳ megabase pairs ۳.۳ x ۱ ۹ billion base pairs diploid size double that misincorporation ۱ ۵ x not proofread ۱ ۲ x escape mismatch repair ۱ ۳ ۱ ۱ thus less than one replication error is fixed per cell division mutation rate per bp ۱ ۹ per base pair per cell division this refers to mutations that are not repaired i.e. they’re fixed thus there are at least six new base changes in each kid that were not present in either parent but this is an underestimate as there’s more since they accumulate in the germ line stem cells as the father ages remember most of these are not in genes from all sources misincorps damage mutation rate per gene from all sources misincorps damage approx ۱ ۵ per gene per cell division human genome contains ۳ ۱ genes thus roughly one new mutation allele is created per cell division most likely recessive dna mismatch repair ۱. muts binds to a mismatched bp ۲. muts dna complex binds mutl ۳. the muts mutl complex translocates along the dna in both directions forming a loop. ۴. on encountering a hemimethylated gatc palindrome the muts mutl complex recrutes muth mmr cont ۵. muts mutl recruits uvrd helicase which in concert with an exsonuclease separates the strands and degradates the nicked strand from the nick to beyond the mismatch. if nick is ۳’ side exsonuclease i ۳’ ۵’ exsonulcease if nick is ۵’ side recj or exsonuclease vii ۵’ ۳’ exsonuclease ۶. dna pol iii fills gap and dna ligase seals nick uracil dna glycosylase and ber an enzyme that removes uracil from dna resulting abasic site is filled in by polymerase uracil in dna comes mainly from deamination of cytosine that may be why dna uses thymine instead of uracil if the uracil isn’t removed it will pair with a causing c g t a transition. ber environmental dna damage the discovery of ner setlow found three mutations in e. coli that rendered the cells sensitive to uv damage. the genes were named uvra uvrb and uvrc for uv resistance. using cell free extracts sancar determined the mechanism of uvrabc which has been refined over the years. the process of uvrabc excision of dna damage is called nucleotide excision repair. uvra is a atp helicase that moves along the dna looking for damage when dna damage is encountered the complex arrests at the site. the dna is bent uvra is released and uvrc is recruited to the complex ner in e. coli continued two single strand nicks are placed to the ۳ side of the dimer ۴ to ۵ nucleotides and to the ۵ side of the dimer ۸ nucleotides helicase ii uvrd unwinds ۱۲ ۱۳ b fragment containing the dimer atp hydrolysis required dna polymerase i fills in the gap dntps required dna ligase seals the single strand break atp hydrolysis to amp required ner in mammalian cells a disease in humans known as xeroderma pigmentosum xp is a rare inherited disease of humans which among other things predisposes the patient to pigmented lesions on areas of the skin exposed to the sun and an elevated incidence of skin cancer. it turns out that xp can be caused by mutations in any one of several genes all of which have roles to play in ner. james cleaver went around and collected cells from hundreds of these patients. he then figured out that the disease was made up of eight genes named xp a through xp g plus one called xp v for variant. there are ۸ xp complementation groups xp a participates in photoproduct recognition and dna binding this binding may be followed by the formation of a quasi stable complex consisting of xpa xpc human single strand binding protein rpa hssb and tfiih which then acts as a nucleation site for binding of the incision excision enzymes. xp b is a ۳’ ۵’ dna helicase that may be involved in unwinding the dna ۵ ward of a damaged base xp c is a single stranded dna binding protein that is essential for repair of the nontranscribed regions of the genome that acts in the initial step of damage recognition. xp d is a ۵ –۳ helicase …

کلمات کلیدی پرکاربرد در این اسلاید پاورپوینت: ‘, ., dna, ۳, ۵, mutation, cell, xp, damage, snp, repair, complex,

این فایل پاورپوینت شامل 84 اسلاید و به زبان انگلیسی و حجم آن 3.36 مگا بایت است. نوع قالب فایل ppt بوده که با این لینک قابل دانلود است. این مطلب برگرفته از سایت زیر است و مسئولیت انتشار آن با منبع اصلی می باشد که در تاریخ 2019/06/07 11:33:52 استخراج شده است.

  • جهت آموزش های پاورپوینت بر روی اینجا کلیک کنید.
  • جهت دانلود رایگان قالب های حرفه ای پاورپوینت بر روی اینجا کلیک کنید.

رفتن به مشاهده اسلاید در بالای صفحه

پاسخی بگذارید

نشانی ایمیل شما منتشر نخواهد شد. بخش‌های موردنیاز علامت‌گذاری شده‌اند *