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genetics test 1, things i need to review: x-inactivation conservation…

- - - - for CC, the clone of Rainbow, the orange X was probably inactivated
- - - - codes for B-galactosidase (lacZ, splits lactose into glucose and galactose) and lactose permease (lacY, transports lactose into cell)
      - promoter: binds RNA polymerase to intiate transcription
      - operator: binds repressor to help control transcription initiation
        
        negative regulation: repressor binds to operator and stops transcription
        
        if lactose is present, it binds to the repressor and prevents it from binding the operator so transcription can occur (lactose = inducer)
        
        when repressor is bound to operator, RNA polymerase can't bind the promoter so transcription can't occur
      - mutations:
        
        lacI-: repressor can't bind to operator so transcription occurs consitutively
        
        lacOc: operator cannot bind repressor so transcription occurs constitutively
        
        lacIs: superrepressor cannot bind lactose but stays bound to operator so no transcription occurs
      - positive regulation: CRP-cAMP complex binding to promoter increases transcription because RNA polymerase can bind stronger. glucose increase causes decrease of cAMP and less CRP-cAMP complex binding to promoter
    - - trp acts as a corepressor for the operon (still negative regulation)
  - - - enhancer is located upstream of promoter (2000 bp cause folding) to aid in binding RNA polymerase by binding even more tf
        
        RNA pol 1: makes rRNA
        RNA pol 2: makes mRNA
        RNA pol 3: makes tRNA
      - nucleosomes must be cleared for tf to bind
    - - 5' methylated cap is added which is critical for ribosomal subunit binding
      - poly-A tail is added to the end of the sequence
      - RNA splicing removes introns and joins exons
        
        spliceosome cuts a splice donor and cuts at splice acceptor so that the ribonucleotides in the intron can be reused
        
        alternative splicing allows for multiple proteins to be made from the same dna sequence
        
        can also create new genes because of gene recombination. but this is not that important unless it happens in sex chromosomes
- - - - activator proteins cover CpG region if no methylation. this keeps the DNA open allowing for RNA polymerase to bind
      - methyl-CpG binding proteins bind and close chromatin structure silencing gene expression cause RNA polymerase can't reach it
      - hemi-methylation (DNA being one new strand and one old) makes it so epigenetics gets passed down in cells
    - - histone acetyl transferases: add acetyl group and favors gene expression
      - histone methyltransferases: methylate histone tail and can favor or hinder gene expression
- - - - non-homologous end joining: create mutations by adding nucleotides to sequence
        homology directed repair: can repair genes using donor DNA but humans create this mutation (donor DNA perfectly fits into break)
      - somatic cell modification: victoria gray's sickle cell disease cure
        
        took cells from bone marrow and turned on the delta globin gene to compensate for a faulty beta globin gene (hemoglobin still gets made then)