DNA synthesis

Dna polymerase - enzymes which catalyze the synthesis of DNA

Helicases - are responsible for unwinding dna

Topoisomerase (such as DNA Gyrase) -

relieve tension caused by helicases by removing supertwists

Replicon - the unit of the genome which is to be replicated.

Nucleosome - histones + DNA

Histones - proteins used for coiling the DNA

SSBs - single-stranded DNA binding protein which keeps the

chromosomes unbound

Polymerase - DNA or RNA synthesizing protein

RNA &DNA primers attach to the lagging strand in order to give it a place to start synthesizing the new DNA.Polymerase or Rnase then remove the primers one at a time & they are replaced by their complementary base pairs.

DNA Ligase will create a phosphodiester bond after the primers are removed, joining together all the Okazaki fragments.

Replisome - The collection of proteins & enzymes which carry out genetic replication. Organisms that replicate faster, may have more than one.

DNA Polymerase I & III can proofread strands of copied DNA & fix incorrectly matched base pairs.

RNA polymerase binding site or Pribnow box site where the RNA polymerase begins to unwind the DNA.

Template strand & non-template strand dna is double-stranded, and only one is used to transcribe mRNA, that is the template. One gene on the template strand includes four portions that aren't used in the translation process, two at each ends. They include the Promoter/Terminator, which act as start & stop signs for the polymerase synthesizing the mRNA. Then on the mRNA we have the leader & trailer sections which also act as start & stop signs but for the ribosome (AUG codon for start). These two are called anti-promoter/trailer when looking at them on the template strand. In-between these is the coding region, the codons which are used in translation.

Regulatory sites are sites where regulatory DNA-recognizing regulatory proteins bind at either stimulate or prevent gene expression

Auxotrophs - a mutant because a certain biochemical pathway isn't producing an endproduct, which must be added to its diet for it to survive

Prototroph the opposite of an auxotroph

Spontaneous mutations occur without any type of exposure and result from errors or sometimes transposons.

Tauterism when one of the base pairs is in an interchangeable structural isomeric form (enol or imino instead of keto). This steric change will cause the hydrogen bonds to occur elsewhere than normal, and A binds to C - G binds to T

Transition mutations occur when a purine is changed for another purine, or a pyrimidine is changed for another pyrimidine. They're common and easily fixed by proofreading.

Transverse mutations occur when a purine is changed for a pyrimidine or vice-versa. They're rare because of the steric issues with pairing purines w/ purines or pyrimidines w/ pyrimidines. May have to do with the size of the molecules…

Depurination is the loss of the base portion of a nucleotide resulting in changes in the way it pairs. Apurinic site or apyrimidinic site is what they are called. Deamination is the change of a uracil to cytosine.

Induced mutations caused by mutagens.

Base analogs structurally similar to bases yet bind differently (5-BU) which can get incorporating into growing polynucleotide

Specific mispairing mutagen changes a base's structure altering its pairing. methyl-nitrosoguanidine adds a methyl group to a guanine, making it pair with thymine. Proof-reading functions have a 1 in 2 chance of fixing this problem, since it doesn't know which base pair was originally there.

intercalating agents insert themselves between base pairs by distorting DNA.

A mutation to the wild type is called a forward mutation, when it's reversed back to the wild type this is called a reversion mutation. And when the forward mutation truly becomes the wild type again this is a back mutation.

Suppressor mutation when the wild type is regained by a second mutation in a different gene. Thus the phenotype is regained, but the genotype remains different.

Most mutations are point mutations, and only affect a single basepair.

silent mutation is the change in a basepair that doesn't affect the product. In this case the old & new codon make the same amino acid, and isn't detectable unless the genome is sequenced.

missense is the change in a base pair which although makes a different amino acid can range from either no change or vast changes in the phenotype.

 
 

The complex which includes the polymerase + accessory proteins is called

• a primosome. It is believed that both the leading & lagging strands are synthesized simultaneously on the same complex. The lagging strand is done in the 5' 3' direction & is discontinuous. The product of the lagging strand is called Okazaki Fragments.
  
• Frameshift mutations changes in the reading frame of the codons. Must be the addition of less than three codons. At three codons, it simply adds the extra amino acid, and may have minimal affect on the functionality and reading frame.
  
• nonsense mutations are early terminations caused by a point mutation. The sooner in the coding portion they are, the more damaging they usually are.
  
  • If the reading frame is restored by another point mutation, then we call that an intragenic suppressor mutation.
    

  DNA methylation is the addition of a methyl group to DNA bases ,done by dna methyltransferases. newer strands lack methyl groups, which helps corrective enzymes differentiate between the old and new strands
  

 
 

Read John Cairns

Direction/adaptive & hypermutations.

Tauterism. Imino enol keto forms.