#Question id: 7755
#Unit 5. Developmental Biology
#Question id: 7757
#Unit 5. Developmental Biology
#Question id: 7761
#Unit 5. Developmental Biology
#Question id: 7764
#Unit 5. Developmental Biology
Cellular senescence
may have evolved to protect organisms against cancer. Instead of dividing out
of control, the cells die. Cellular senescence appears to be regulated by
several tumor suppressor genes, especially p53.what is the most appropriate
reason behind this,
1) Transcription
factor p53 is thought to suppress tumorigenesis by causing cell arrest and
senescence in response to short telomeres, DNA damage, and viral or external
signals to divide
2) This factor can
stop the cell cycle, cause cellular senescence in rapidly dividing cells,
instruct genes to initiate cellular apoptosis, and activate DNA repair enzymes.
3) Induction of apoptosis or cellular senescence by p53 always beneficial.
#Question id: 7765
#Unit 5. Developmental Biology
The enzyme complex or gene that maintains telomere integrity is________, which acts as an antisenescence complex. Mice and humans with its deficiencies age prematurely (Mitchell et al. 1999). Overexpressing or reactivating it in senescent cells extends longevity in mice without increasing cancer,
#Question id: 7766
#Unit 5. Developmental Biology
The relationship between shortened telomeres and stem cell
depletion has been seen in degenerative diseases such as mouse muscular
dystrophy,
I) When____ is activated by damaged telomeres, DNA replication halts, and if the repair doesn’t work, apoptosis is initiated. If the cell is a stem cell or some other rapidly replicating cell, this will reduce the numbers of cells produced, and the lack of stem cells will produce an “aged” phenotype.