Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sem 1 > 22. Cell Determination and Cell Senescence > Flashcards

22. Cell Determination and Cell Senescence Flashcards

1
Q

Describe cell determination?

A

Process whereby the cell fate becomes stable. It is followed by cell differentiation. When a cell chooses a particular fate it is said to be determined. Implies a stable change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe cell determination? (4pts)

A
  1. Process by which portions of the genome are selected for expression in different embryonic cells.
  2. Occurs in totipotent, embryonic stem cells.
  3. A result of asymmetric segregation of cytoplasmic determinants.
  4. Responsible for assigning the fate of the cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe cell differentiation? (4pts)

A
  1. Process by which a cell becomes specialised in order to perform a specific function.
  2. Follows cell determination
  3. A result of differential gene expression
  4. Responsible for the functional specialisation of the cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe cell differentiation? (4pts)

A
  1. Process by which a cell becomes specialised in order to perform a specific function.
  2. Follows cell determination
  3. A result of differential gene expression
  4. Responsible for the functional specialisation of the cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe Asymmetrical cell division? (3pts)

A
  1. Asymmetrical cell division is due to differential distribution of cytoplasmic molecules (proteins or mRNAs) within a cell before it divides.
  2. The 2 new daughter cells have different fates therefore have a different gene expression profile.
  3. Cells with p granules will generate germ cells. Cells with no p granules will give rise by division to other types of cells in the organism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is cell determination caused? (2pts)

A
  1. Cell determination is caused by inductive signals from neighbouring cells.
  2. One group of cells influences the development of another group of cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe Pioneer factors? (4pts)

A
  1. Transcription factors that access closed chromatin, remodel it and imitate cell-fate.
  2. Highly expressed in embryonic stem cells and needed to maintain their pluripotency.
  3. Can activate or inhibit gene expression via histone modification and DNA methylation.
  4. Pioneer factors together with co-factors are key in cell-fate decision making.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Cell senescene?

A

Deterioration of the cells due to age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Apostosis?

A

Programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe Cell senescene? (5pts)

A
  1. Cell senescene refers to the deterioration of cells due to age.
  2. Takes place during the process of ageing.
  3. Irreversible arrest of cells during cell profileration is the significant feature
  4. It is caused by oxidative stress, DNA damage and alternation of genetic expression
  5. It is regulated by genes involved in ageing mechanisms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe Apostosis? (5pts)

A
  1. Apostosis is programmed cell death
  2. Its role is to balance the cell number at a constant rate
  3. Chromosome condensation is the significant feature
  4. It is caused by different physiological and pathological conditions.
  5. Apoptosis is regulated by intracellular proteolytic mechanisms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the cell lifespan?

A
  • Is the total number of doublings that a cell population goes through before senescence. The length of time for which a cell exists.
  • Hayflick and Moorhead found out that normal foetal fibroblasts only reached a maximum of 50 cell populations doublings before becoming senescence. This is the Hayflick limit.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the Hyaflick limit?

A

The number of times that a normal human cell population will divide before cell division.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe normal cells and immortal cells?

A

Normal cells have a finite lifespan as opposed to immortal cells. The only immortal cells are cancer cells which can divide forever and never reach their hayflick limit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the effects of cellular senescene? (3pts)

A
  1. Morpholoigcal changes I
  2. Biochemical changes
  3. Chromatin changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe Morphological changes? (5pts)

A
  1. Cells become larger
  2. Cells display increased granulaity
  3. Cells flatten out
  4. Cell borders tend to vanish
  5. Cytoplasm becomes more vacuole-rich.
16
Q

Describe Biochemical changes? (2pts)

A
  1. Increased perinucleur activity of SA-B-galactosidase.

2. Increases protein levels of senescence markers such as p53.

16
Q

Describe Biochemical changes? (2pts)

A
  1. Increased perinucleur activity of SA-B-galactosidase.

2. Increases protein levels of senescence markers such as p53.

17
Q

Describe Chromatin changes? (2pts)

A
  1. Focal HP1 recruitment

2. Senescene associated heterochromatin foci.

18
Q

Describe a Telomere?

A

Regions at the end of chromosome composed of TTAGGG DNA sequences whose function is to preserve chromosome integrity during each DNA replication thus preventing DNA damage (constitutive heterochromatin)

19
Q

Describe the loss of telomeres?

A

Loss of telomere by chromosome breakage results in unstable chromosome ends that can fuse with other broken chromosomes or be involved in recombination events or be degraded. It can also involve the damage of telomere flanking genes.

19
Q

Describe the loss of telomeres?

A

Loss of telomere by chromosome breakage results in unstable chromosome ends that can fuse with other broken chromosomes or be involved in recombination events or be degraded. It can also involve the damage of telomere flanking genes.

20
Q

Describe telomeric DNA?

A

Telomeric DNA is associated with a 6-member protein sheltrin complex that facilitates the formation of loops which cap the chromosome end.

21
Q

Describe Progressive Telomere shortening?

A

Progressive telomere shortening occurs in all dividing normal cells mainly due to the incomplete DNA lagging strand. The lagging strand is always shorter than the leading strand. Every time a cell divides telomeres shorten due to this incomplete lagging strand DNA synthesis.

22
Q

What is telomerase?

A

Telomerase is a ribonucleoprotein which replicates telomeric DNA by reverse transcribing DNA hexamers from RNA using its RNA subunit and its protein component TERT.

23
Q

Describe the activity of Telomerase? (2pts)

A

Telomerase elongates telomeric DNA by repetition of a two-step cycle:

  1. Synthesis
  2. Translocation
24
Q

Describe the activity of Telomerase?

A
  1. In the lagging strand telomerase binds the first few nucleotide of the template to the last telomere sequence of the chromosome
  2. It adds a new telomere repeat complementary to the telomere sequence which recognises the new 3 prime end of the telomere to the template.
  3. Process is repeated.
25
Q

What does telomerase do to telomere shortening?

A

Telomerase reverses telomerase shortening because it is able to elongate telomerase.

26
Q

Describe telomere length? (3pts)

A
  1. Telomere length is highly variable and telomerase activity is normally absent from adult somatic cells except for proliferative tissues such as blood, skin and intestine.
  2. Replicative senescne is triggered in normal cells when telomeres get short.
  3. Telomere length is a way of counting cell division.
27
Q

What happens to cells which express TERT?

A
  1. Germline cells and sperm cell all express TERT so they maintain full length telomeres. Germlie is immortal so cells can divide forever
  2. Cancer cells activate telomerase leading to uncontrolled replication and survival. Nearly all cancer cell lines in culture express TERT so they are immortal.
28
Q

Describe advanced cancer cells?

A

Advanced cancer cells have usually bypassed cell senescence. Some of the common abnormalities found in cancer cells are those leading to defective senescence and immorality.

29
Q

What is the evidence for telomeres? (7pts)

A
  1. Telomere length is typically very short in people aged above 100.
  2. Telomeres shorten as we age, The longer they are the healthier the person is.
  3. p16 and other senescence-related proteins are expressed increasingly in ageing tissues.
  4. Telomere length at birth varies between people- genetically linked to age at death
  5. Defective genes for telomerase subunits give syndromes with premature ageing and early death.
  6. P16 locus also genetically associated with human senile defects.
  7. Telomere kits detect the biological age of cells and predict how long you will live for.
30
Q

Describe Telomeres and stem cells? (3pts)

A
  1. Embryonic stem cells express TERT as they are naturally immortal.
  2. Some adult stem cells have some telomerase activity but in general too little to make the cells immortal.
  3. Telomeres shorten less per division is somatic stem cells than in other stem cells but they do shorten so most somatic stem cells do senescence gradually.
31
Q

Describe bone marrow and cell senescence

A

Older people show decreased immunity, increased bone marrow failure, decreased success rate as bone marrow doners. Reduced proliferative ability of marrow stem cells.

32
Q

Describe hair greying and cell senescnce?

A

Hair greying is linked to decreased melanocyte stem cell maintenance in hair follicles

33
Q

Describe the healing ability of skin?

A

With age, increased risk of skin ulcers occur. Proposed to be due to senescence in dermal fibroblasts.

Sem 1 (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions