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TLS Online TPP Program

#Question id: 13161

Which of the following mechanism depends on the activation of heterotrimeric G proteins?

#Unit 4. Cell Communication and Cell Signaling
  1. During actin filament formation, the inactive formin is activated when its Rho-binding domain (RBD) binds to membrane-bound active Rho-GTP, resulting in exposure of the formin’s FH2 domain, which can then nucleate the assembly of a new actin filament.
  2. Rod cells sense light with the aid of a light-sensitive rhodopsin which is coupled to transducin. On absorption of a photon, the retinal moiety of rhodopsin is immediately converted from the cis isomeric form to the all-trans isomeric form, causing a conformational change that allows rhodopsin to bind the α subunit of transducin.
  3. Ras proteins are “switch” proteins and not directly linked to cell-surface receptors. Ras activation is accelerated by a guanine nucleotide exchange factor (GEF), which binds to the Ras∙GDP complex, causing dissociation of the bound GDP.
  4. During the regulation of microfilament organization, Cdc42 act as molecular switches, inactive in the GDP-bound state and active in the GTP-bound state.
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TLS Online TPP Program

#Question id: 7760

#Unit 5. Developmental Biology

In general, the hormones that regulate senescence can be divided into two basic categories based on their most commonly observed effects:
I) positive (promoting) senescence regulators and
II) negative (repressing) senescence regulators
a) Hormones involved-Ethylene, Abscisic acid (ABA)
b) Hormones involved-Brassinosteroids (BRs), Salicylic acid (SA), Jasmonic acid (JA)
c) Hormones involved-Cytokinin, Auxin, Gibberellin (GAs)
Select correct combinations from given hormones which are involved in regulators?
TLS Online TPP Program

#Question id: 7761

#Unit 5. Developmental Biology

Correct sets of genes are well known to be involved in aging and its prevention, and each set appears to be conserved between phyla and even kingdoms. 
a. DNA repair enzymes
b. proteins of the insulin signaling pathway
c. proteins in the mTORC1 signaling pathway
d. chromatin remodeling enzymes
TLS Online TPP Program

#Question id: 7762

#Unit 5. Developmental Biology

Correlation between life span and the ability of fibroblasts to repair DNA in various mammalian species, Repair capacity is represented in autoradiography by the number of grains from radioactive thymidine per cell nucleus. According to graph, which factor exist on x-axis ? Note that the y-axis (life span) is logarithmic.
TLS Online TPP Program

#Question id: 7763

#Unit 5. Developmental Biology

Two major sources of mutation are radiation and reactive oxygen species (ROS).The reactive oxygen species hypothesis for aging postulates that 
1) Senescence results from the accumulation of DNA, lipid, and protein damage inflicted by ROS of mitochondrial origin; and
2) Mitochondria of long-lived species should produce high ROS than do mitochondria of short-lived species.
3) the capacity of mitochondria to consume ROS might distinguish long-lived species from short-lived species, rather than differences in ROS generation. 
TLS Online TPP Program

#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.
TLS Online TPP Program

#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,