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Ch 2: Cellular responses to stress etc > Cellular Aging > Flashcards

Cellular Aging Flashcards

1
Q

Cellular aging is regulated by?

A

Genes that are evolutionarily conserved from yeast to worms to mammals.

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2
Q

Briefly outline the process behind cellular aging

A

Genetic abnormalities and accumulation of cellular and molecular damage due to exogenous influences cause a progressive decline in cellular function and viability.

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3
Q

Several mechanisms, some ____ _______ and others _________ _________ are believed to play a role in aging.

A

Cell intrinsic

Environmentally induced

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4
Q

What 4 mechanisms play a role in cellular aging?

A
  1. DNA damage
  2. Cellular scenescence
  3. Defective protein homeostasis
  4. Deregulated nutrient sensing
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5
Q

How many new mutations per year is the average haemopoietic stem cell expected to suffer?

A

14

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6
Q

Patients with Werner syndrome show premature aging due to a defective DNA ______. This causes rapid _______ of _______ damage that may mimic the injury that normally accumulates during cellular _______.

A

Helicase
Accumulation
Chromosomal
Aging

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7
Q

Other disorders in which patients display some of the manifestations of aging at an increased rate.

A

Bloom syndrome

Ataxia-telangiectasia

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8
Q

In Bloom syndrome and Ataxia-Telangiectasia, mutated genes encode proteins involved in?

A

Repairing double-strand breaks in DNA

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9
Q

All normal cells have a limited capacity for?

A

Replication

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10
Q

After a _______ number of divisions, cells become __________ in a terminally __-______ state, known as ________ ______.

A

Fixed
Arrested
Non-dividing
Replicative senesence

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11
Q

Aging is associated with

A

progressive replicative senescence of cells.

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12
Q

T or F: Cells from children can undergo fewer rounds of replication than cells of older people.

A

False

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13
Q

What are the 2 mechanisms underlying cellular senescence?

A
  1. Telomere attrition

2. Activation of tumour suppressor genes

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14
Q

What are telomeres?

A

Short repeated sequences of DNA present at the ends of linear chromosomes

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15
Q

What are telomeres important for?

A
  1. Ensuring complete replication of chromosome ends

2. Protecting the ends from fusion and degradation

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16
Q

What happens to telomeres as somatic cell replication occurs?

A

A small section of the telomere is not duplicated each time and telomeres become progressively short.

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17
Q

What is the consequence of telomere shortening?

A

The ends of the chromosomes are no longer protected and are seen as broken DNA, signalling cell cycle arrest

18
Q

How is telomere length maintained?

A

Nucleotide addition mediated by an enzyme called telomerase

19
Q

What is telomerase?

A

A specialised RNA-protein complex that uses its own RNA as a template for adding nucleotides to the ends of chromosomes.

20
Q

Telomerase activity is expressed in which cells?

A 
Germ cells
Stem cells (low level)
21
Q

Telomerase activity is absent in which cells?

A

Most somatic tissues

22
Q

Therefore, as most somatic cells age, their telomeres become shorter and they exit the cell cycle. This results in?

A

An inability to generate new cells to replace damaged ones.

23
Q

In immortalised cancer cells, telomerase is usually _______ and telomere length is __________.

A

Reactivated

Stabilised

24
Q

What diseases has premature telomere shortening been associated with?

A

Pulmonary fibrosis

Aplastic anaemia

25
Q

Which tumour suppressor genes are correlated with chronologic age?

A

p16

INK4a

26
Q

Where are p16 and INK4a located?

A

CDKNA2A locus

27
Q

What does p16 do?

A

Controlling G1 to S phase progression during the cell cycle.

28
Q

What does p16 protect the cell from?

A

Uncontrolled mitogenic signales

29
Q

Protein homeostasis involves 2 mechanisms.

A
  1. Maintenance of proteins in their correctly folded conformations
  2. Degradation of misfolded proteins by the autophagy-lysosome system and ubiquitin-proteasome system
30
Q

Maintenance of protein conformation is mediated by?

A

Chaperones eg heat shock protein family

31
Q

What is rapamycin?

A

mTOR inhibitor

32
Q

What role does rapamycin play in cellular aging?

A

Promotes autophagy that probably prevents accumulation of misfolded proteins which would otherwise trigger apoptosis.

33
Q

T or F: caloric restriction decreases longevity.

A

False

34
Q

2 pathways by which caloric restriction may increase longevity

A
  1. Reducing signaling intensity of IGF-1 pathway

2. Increasing sirtuins

35
Q

What role does IGF-1 play in cellular aging?

A

IGF-1 informs cells of the availability of glucose, promoting an anabolic state as well as cell growth and replication, via multiple downstream targets, the 2 most pertinent being AKT and its downstream target, mTOR

36
Q

What is IGF-1?

A

Produced by many cell types in response to growth hormone secretion by the pituitary, mimics intracellular signaling by insulin.

37
Q

What are sirtuins?

A

A family of NAD-dependent protein deacetylases.

38
Q

How many types of sirtuins are there?

A

At least 7 type in different cellular compartments with non-redundant functions.

39
Q

What are the functions of sirtuins?

A

Adapt bodily functions to environmental stresses including food deprivation and DNA damage.

40
Q

What role do sirtuins have in cellular aging?

A

Promote the expression of several genes whose products increase longevity.

41
Q

What are the actions of proteins produced by sirtuins?

A

Inhibit metabolic activity
Reduce apoptosis
Stimulate protein folding
Inhibit harmful effects of oxygen free radicals
Increase insulin sensitivity and glucose metabolism

Ch 2: Cellular responses to stress etc (3 decks)

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