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M2M Biochemistry and molecular biology > Gene Expression Shred Fest I LO > Flashcards

Gene Expression Shred Fest I LO Flashcards

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1
Q

what determines the amount of protein within each cell? (4)

A
  1. amount of mRNA
  2. frequency of mRNA translation
  3. stability of the protein
  4. Rate of degradation of protein
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2
Q

what is the most important mechanism for determining gene expression and amount of protein synthesized?

A

transcription initiation

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3
Q

what are the 2 basic components important to eukaryotic gene expression?

A
  1. DNA control elements-part of DNA that acts locally (cis)

2. transcriptional activators/repressors that act on other genes to regulate their transcription (trans)

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4
Q

where do DNA control elements act?

A

locally, transcription factors bind to elements that control expression of that gene

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5
Q

what are the 3 DNA control elements?

A
  1. TATA box/initiator (promoter)
  2. promoter proximal element
  3. enhancer
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6
Q

what is the TATA box?

A

located 25-35 bp upstream of transcription start, determines site of transcription initiation and directs binding of RNA pol II

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7
Q

what is the promoter proximal element?

A

200 bps upstream of start site and about 20 bps long, helps regulate transcription

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8
Q

what is the enhancer?

A

200-tens of thousands bps upstream or downstream from promoter or within an intron

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9
Q

what binds at the TATA box?

A

general transcription factors like TATA binding protein

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10
Q

what are the 3 diseases associated with mutations in the DNA control elements?

A
  1. Thalassemias
  2. Hemophilia B-Leyden
  3. Fragile X-Syndrome
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11
Q

what does an enhancer do?

A

binding of proteins enhances transcription levels

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12
Q

what is a silencer?

A

Section of DNA that binds transcription regulating factors called repressors

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13
Q

how does a silencer work?

A

when repressors bind, RNA polymerase is prevented from initiating transcription, thus lowers or eliminates transcription

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14
Q

how is thalassemias inherited?

A

autosomal recessive

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15
Q

what is thalassemias?

A

blood disease that occurs due to different genetic mutations such as mutation or deletion

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16
Q

what mutation causes B-Thalessemias?

A

B-globin promoter mutation causing decreased transcription of this protein but not complete loss of this protein

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17
Q

what mutation causes yDB thalessemias?

A

deletion of locus control region (LCR) of B-globin gene cluster, very severe form because LCR directly regulate expression of all genes in that cluster

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18
Q

what chromosome is hemophilia B leyden linked to?

A

X

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19
Q

what does hemophilia B leyden affect?

A

blood clotting

20
Q

how does hemophilia B leyden affect males?

A

have 1% of normal factor IX active until puberty, once androgen receptor becomes active, produce about 60% of normal factor IX

21
Q

what is the presentation of fragile X syndrome?

A

mental retardation, dysmorphic facial features, postpubertal macroorchidism (abnormally large testes)

22
Q

why does fragile-X syndrome develop?

A

expansion of CGG trinucleotide repeats in the 5’ region of FMR1 gene on X chromosome. normal humans have about 6-55 repeats but fragile X syndrome patient have between 230-4000 repeats

23
Q

why does increasing the amount of CGG repeats cause fragile X syndrome?

A

there is an increase in the methylation of cytosine residues in CpG islands of FMR1 promoter, methylation then causes silencing of FMR1 gene

24
Q

what is the severity of fragile X syndrome directly related to?

A

the number of CGG repeats

25
Q

what does the mutation in hemophelia B leyden disease prevent?

A

binding of appropriate transcriptional activators to Factor IX gene

26
Q

what are transcriptional factors?

A

proteins encoded by one gene that act on other genes to regulate their transcription (activators and repressors)

27
Q

what are the 2 classes of activators and repressors?

A
  1. sequence-specific DNA binding proteins

2. Co-factors

28
Q

what is a sequence-specific DNA binding protein?

A

protein that binds to the promoter or enhancer elements in their target genes to regulate transcription

29
Q

how do sequence-specific DNA binding protein binds to the DNA?

A

insert alpha helices into the major groove of DNA

30
Q

what are co-factors?

A

proteins that bind to sequence-specific DNA binding proteins rather than directly to DNA

31
Q

what are the 4 families of sequence-specific DNA binding proteins?

A
  1. homeodomain proteins (helix-turn-helix)
  2. Zinc-finger proteins
  3. basic leucine zipper proteins (bZIP)
  4. Basic helix-loop-helix motif (bHLH)
32
Q

What is the difference between a DNA binding domain and an activation domain?

A

DNA binding domain protein binds directly to the DNA molecule. Activation domain has a protein to protein interaction that modifies transcription

33
Q

what are the characteristics of a DNA binding domain?

A
  • highly structured
  • evolutionarily conserved
  • structure allows them to bind directly to the DNA molecule
34
Q

what are the characteristics of an activation/repressor domain?

A
  • not highly conserved
  • not very structured until they bind cofactors or general transcription factors
  • recruits additional factors to upregulate or downregulate transcription
35
Q

what are some examples of homeodomain proteins (helix-turn-helix)?

A

Hox family (embryologic development), Pit1 (pituitary development and hormone expression), msx (limb pattern formation)

36
Q

what are some examples of zinc-finger proteins?

A

nuclear receptors such as estrogen, androgen receptors

37
Q

what does a basic leucine zipper proteins and basic helix-loop-helix proteins require to bind to DNA?

A

homodimerization

38
Q

what are some examples of basic leucine zipper proteins?

A

c-fos and c-jun (proto-oncogene)

39
Q

what are some examples of helix-loop-helix (bHLH) proteins?

A

MyoD (muscle differentiation), myogenin (skeletal muscles development and repair), and MyF5 (muscle differentiation)

40
Q

what is craniosynotosis and what mutation causes it?

A
  • premature closing of one or more sutures in the skull.
  • mutation in homeodomain of protein MSX2 (required in proper cranio-facial development)
  • proline to histidine amino acid substitution
  • one amino acid change in binding domain makes bind more strongly causing “gain of function” or “hypermorphic allele” leading to suture closure
41
Q

what is the presentation of androgen insensitivity syndrome (AIS)?

A

feminization, undermasculinization of external genetalia at birth, abnormal secondary sexual development in puberty, and infertility

42
Q

where is the mutation in androgen insensitivity syndrome?

A

DNA binding domain or ligand binding domain of androgen receptor (zinc finger binding domain), causes decreased sensitivity to androgen

43
Q

what is Waardenburg syndrome type II?

A

mutation in MITF gene, renders gene nonfunctional, affects transcription of genes important in pigmentation and in hearing

44
Q

what is combinatorial control?

A

when thousands of transcription factors can regulate tens of thousands of genes

45
Q

what do activators and repressors regulate?

A
  • assembly of initiation complexes
  • rate of initiation of transcription
  • changes in chromatin structure influencing binding to promoters
46
Q

what is dimerization?

A

where multiple DNA binding factors (zinc finger etc) come together at binding sites and illicit different gene responses based on which factors are present in a cell at a certain time

47
Q

what does heterodimerization allow for (2)?

A
  • recognize different DNA sequences allows recognition of new DNA sites
  • new combinations of activation domains to be brought together

M2M Biochemistry and molecular biology (19 decks)

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