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BMS > Homeobox Genes > Flashcards

Homeobox Genes Flashcards

1
Q

The important question of “how do we develop our body plan” has been extensively studied in which two model organisms?

A

Drosophila Melanogaster (fruit fly) and Mus musculus (house moue)

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2
Q

One advantage of using the fruit fly is that they have a short generation time. How long does it take for the fruit fly to go from egg to adult?

A

14 days

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3
Q

One advantage of using the mouse is that they are very amenable to genetic manipulations such as

A

Gen knockouts and knock ins, and transgenics

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4
Q

Deleting a gene via embryonic stem (ES) cells

A

Gene knockout

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5
Q

Replacing one version of a gene with another via embryonic stem cells

A

Gene knockin

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6
Q

Adding extra copis of any gene

A

Transgenics

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7
Q

In early mouse development, the group of cells in the center of the blastocyst is called the

A

Inner cell mass (ICM)

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8
Q

Pluripotent for the embryo

A

ICM cells

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9
Q

Cells in the outer epithelium are committed to generate part of the

A

Placenta

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10
Q

Can be isolated and grown in cultures

A

ICM cells

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11
Q

These mice ICM cells retain their pluripotency in vitro and are called

A

Embryonic stem (ES) cells

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12
Q

Enable a mouse to be generated that has a specific DNA change that we want to study

A

The pluripotent ES cells

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13
Q

If you delete a gene in the ES cells then a mouse can be generated that contains all the genes in the genome except the specific one that was deleted. These mice are called

A

Kock-outs

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14
Q

If you introduce more subtle specific changes into the DNA such as replacing a wild type sequence with a specific mutation, then you get mice called

A

Knock-ins

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15
Q

The insertion of DNA into the genome. DNA is not deleted, rather, extra copies of a gene are added. Mice that undergo this process are called

A

Transgenics

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16
Q

How are transgenics made?

A

DNA injected into nuclei of fertilized egg

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17
Q

Mutations where one structure is replaced with another or is duplicated

A

Homeotic Mutations

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18
Q

Homeotic mutations were known to exist since the 1930’s, but the genes responsible for these defects were not known until the development of

A

DNA recombinant technology (1980’s)

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19
Q

Cloning of genes responsible for homeotic mutations was first achieved in

A

Drosophila

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20
Q

Sequence homology was observed between genes responsible for different homeotic mutations. This DNA sequence was termed the

A

Homeobox

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21
Q

The homeobox is 180 bp in length and encodes a protein called a homeobox transcription factor. The part of the protein that binds DNA is called the

A

Homeodomain

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22
Q

Encode transcription factors that typically initiate a cascade of gene expression necessary for the development of a body structure or cell type

A

Homeobox genes

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23
Q

Homeobox proteins are transcription factors that bind DNA in a sequence specific manner. All homeobox proteins bind

A

AT rich elements in promoters and enhancers

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24
Q

The homeodomain amino acid sequence is responsible for binding and recognizing the AT rich binding site found in many

A

Promoters and Enhancers

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25
Q

The homeodomain protein sequence is comprised of 3 alpha helices. Which helix makes direct contact with the DNA?

A

The 3rd helix

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26
Q

All homeobox transcription factors bind

A

AT rich DNA sequences

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27
Q

In vitro, homeobox proteins demonstrate little or no specificity. However, in vivo, homeodomain transcription factors form protein complexes to determine

A

Specificity (very important in vivo or legs would be arms)

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28
Q

Only makes up a small portion of the homeobox transcription factor

A

Homeodomian

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29
Q

Other proteins bind to different parts of homeobox transcription factors to modify function and help determine

A

Specificity

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30
Q

There are many genes that contain homeobox sequences. These genes are broken into which two classes?

A
  1. ) Hox genes

2. ) Genes that when mutated, do not result in structural change

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31
Q

Genes that when mutated result in homeotic transformations

A

Hox Genes

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32
Q

The second class of homeobox sequences are not physically

A

Clustered together

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33
Q

Control the patterning of cell types, and mutations in these genes often result in the loss or gain of parts of cell types

A

Second class genes

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34
Q

Clustered into 4 physically linked groups in humans

A

Hox genes

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35
Q

In the evolution from drosophilia to mouse to human, there is a consistent increase in the number of

A

Homeobox genes (i.e. from 1 to 4)

36
Q

Function in patterning the body axis

A

Hox genes

37
Q

Expressed in specific embryonic domains and function in the generation of that particular body part

A

Hox genes

38
Q

Hox genes are positioned on the chromosome in the same order in which they are expressed. Where are the following genes expressed?

  1. ) Genes positioned 5’ in the Hox cluster
  2. ) Genes positioned 3’ in the Hox cluster
A
  1. ) Posterior domain

2. ) Anterior domain

39
Q

How many Hox clusters are present in mice and humans?

A

4 (Hox a, b, c, and d)

40
Q

Homologous genes between species

A

Orthologs

41
Q

Homologous genes within a species

A

Paralogs

42
Q

Expressed in the developing neural tube as well as the flanking somites

A

Mouse Hox genes

43
Q

Body segments containing the same internal structures

-seen in embryonic mouse

A

Somites

44
Q

Somite expression is always shifted

A

Posteriorly

45
Q

Hox genes further 3’ have more anterior expression boundaries. This is called

A

Spacial co-linearity

46
Q

3’ Hox genes are also expressed earlier in development than 5’ genes. This is called

A

Temporal co-linearity

47
Q

Different groups of cells express distinct patterns of Hox genes depending on their position along the anterior-posterior (A-P) axis. This is called the

A

Hox code

48
Q

Dictates the development of different structures along the A-P axis

A

Hox code

49
Q

Hox genes are transcription factors, so they will determine which downstream genes get turned

A

On

50
Q

These downstream genes will in turn determine the developmental structures that will be

A

Derived

51
Q

Loss of function Hox mutations (knock-outs) lead to

A

Anterior transformations

52
Q

Gain of function Hox mutations lead to

A

Posterior transformations

53
Q

Have less severe phenotype than double or triple mutants

-an example of redundancy or overlapping function

A

Single mutants

54
Q

Function as transcription factors so they either initiate or repress downstream gene expression

A

Hox genes

55
Q

One function of Hoxa2 and Hoxb2 is to initiate gene expression responsible for the generation of

A

Cervical vertebrae C2

56
Q

Hoxa3, Hoxb3 and Hoxd3 are expressed in a more posterior compartment and one of their functions is to initiate gene expression responsible for the generation of

A

Cervical vertebrae C3

57
Q

Hoxa2, Hoxb2, Hoxa3, Hoxb3 and Hoxd3 are all co-expressed in the same set of cells along the A-P axis. What would happen if a deletion knocked out Hoxa3, b3, and d3?

A

A second C2 vertebrea would form instead of a C3

58
Q

Initiates the expression of genes responsible for the generation of C4 vertebrae

A

Hoxd4

59
Q

Every Hox gene works together with the Hox genes located

A

Downstream in the cluster

60
Q

In a transgenic mouse with misexpression of Hoxd in a more anterior structure, we would see

A

2 C4 vertebrae and no C3

61
Q

Hox gene expression extends as far anterior as the

A

Hindbrain

62
Q

Formation of Drosophila head structures is controlled by a homeobox transcription factor called

-NOT part of the Hox cluster

A

Orthodenticle (Otd)

63
Q

No hox genes are expressed in the

A

Anterior head structures

64
Q

Mice and humans have 2 Otd analogs called

A

Otx1 and Otx2

65
Q

Drosophila Otd is expressed in anterior blastocyst in a region of the embryo that will give rise to

A

Anterior brain structures

66
Q

Drosophila null mutants for Otd result in embryos without

A

Head and brain structures

67
Q

Mice with Otx1 knockouts survive embryogenesis, but have

A

Smaller brains

68
Q

Results in lethality and the deletion of forebrain structures during early mouse development, which is similar to the Otd Drosophila phenotype

A

Otx2 knockout

69
Q

These studies demonstrate that Otx or Otd transcription factors are essential for regulating gene expression necessary to generate

A

Anterior (head/forebrain) brain structures

70
Q

Turn on a series of downstream genes, which then function together to generate head/forebrain structures

A

Otc and Otx1/2

71
Q

Situated at the top of a transcriptional cascade and NO other transcription factor in the genome is capable of performing this function

A

Otd and Otx1/2

72
Q

Overexpression of Otd or Otx results in a

A

Larger brain

73
Q

When mouse Otx1 was expressed in drosophila in place of Otd, the result was

A

Larger brains (shows functional redundancy)

74
Q

What hapened when fly Otd was inserted into a mouse in place of Otx1?

A

The brain size was equal to wild type

75
Q

Fly Otd is functionally equivalent to

A

Mouse Otx1

76
Q

Caused by diseases such as amyotrophic lateral sclerosis (ALS), spinal muscular atrophy, progressive muscular atrophy or by injury to the spinal cord

A

Motor neuron damage

77
Q

Can generate mature cell types in vitro

A

ES cells

78
Q

Basic science has identified a cascade of transcription factors required for

A

Motor neuron generation

79
Q

Researchers have used this knowledge to generate motor neurons in culture from

A

ES cells

80
Q

A transcription factor code has been identified for generating embryonic stem cells. These genes can convert other cell types into ES cells. What are the genes?

A

OCT4 and NANOG (homeobox TF’s), SOX2, C-MYC, and KLF4

81
Q

The forced expression of these genes in skin fibroblasts converts them to

A

Induced pluripotent stem cells (iPS cells)

82
Q

Have been implicated in human disease

A

Homeobox genes

83
Q

Important for patterning the vertebrate limbs

A

Hox genes

84
Q

Mutations in HOXD13 in both humans and mice result in digit malformations known as

A

Synpolydactyly

85
Q

Observed in individuals with hand malformations

A

Missense mutations in HOX13D (3rd alpha-helix)

86
Q

Protein modeling studies indicated that these amino acid changes affect the 3-D configuration of the

A

Hox gene

87
Q

Protein-DNA binding assays demonstrate that the the missense mutations affect

A

DNA binding

BMS (62 decks)

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