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#stress response

13 public questions tagged with this topic.

Plant tissue culture 1

Abscisic acid is known as:

Abscisic acid designated as stress hormone and growth inhibitor originates from carotenoid pathway, cleavage of 9 cis violaxanthin and neoxanthin by NCED dioxygenase to xanthoxin then converted by ABA2 short chain dehydrogenase and AAO3 aldehyde oxidase to ABA. Under drought salinity cold endogenous levels rise sharply triggering PYR PYL RCAR receptor family that sequesters PP2C phosphatases ABI1 ABI2 releasing SnRK2 kinases OST1 to phosphorylate targets including bZIP transcription factor ABI5 inducing late embryogenesis abundant LEA genes, anion channel SLAC1 causing stomatal closure reducing transpiration, and enzymes for osmolyte synthesis proline betaine. ABA antagonizes gibberellin by stabilizing DELLA repressors enforcing dormancy and preventing precocious germination vivipary. In tissue culture ABA 1-10 micromolar improves somatic embryo quality preventing secondary embryogenesis, induces desiccation tolerance for synthetic seed storage, synchronizes maturation and enhances acclimatization by promoting cuticular wax deposition. Catabolism via CYP707A hydroxylases maintains homeostasis fine tuning stress response and developmental transitions crucial for embryo physiology.

Ref: Cutler et al., Annu Rev Plant Biol 2010 ABA signaling; NCBI NBK541119 ABA.

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Microbial Physiology

The sigma factor σ³² in bacteria regulates:

Transcription initiation specificity depends on sigma factors that bind core RNA polymerase and recognize distinct promoter elements at minus 35 and minus 10 regions. Among seven sigma factors in Escherichia coli, sigma32 encoded by rpoH gene governs heat shock regulon comprising chaperones and proteases. Under optimal temperature DnaK and DnaJ chaperones bind sigma32 delivering it to membrane protease FtsH for rapid proteolysis keeping cellular level extremely low and half-life about one minute. Heat-induced protein misfolding titrates DnaK and DnaJ away from sigma32, stabilizing it and enhancing translation of rpoH mRNA via melting of inhibitory secondary structure that normally sequesters ribosome binding site. Free sigma32 then associates with core polymerase to transcribe about 90 genes including dnaK, dnaJ, grpE, groEL, groES, clpB, lon and hslVU. Oxidative stress response uses OxyR and SoxRS regulators, antibiotic resistance uses MarA, quorum sensing uses LuxR homologs with autoinducers, distinguishing sigma32 as dedicated heat stress sigma factor integrating protein folding status into transcriptional reprogramming to restore proteostasis and survival.

Ref: Lodish et al., Molecular Cell Biology, 8th ed., Chapter 10: Sigma Factor σ32 and Heat Shock Regulation.

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Translation in Prokaryotes and Eukaryotes

Phosphorylation of eIF2α leads to

Phosphorylation of eIF2 alpha at Ser51 sequesters eIF2B pentameric guanine nucleotide exchange factor that normally regenerates active ternary complex eIF2 GTP Met-tRNAi from inactive GDP form. Since cellular eIF2B concentration is about tenfold lower than eIF2, even modest phosphorylation proportion immobilizes most eIF2B, collapsing ternary complex availability. Consequently global cap-dependent translation is rapidly shut down, conserving energy and reducing endoplasmic reticulum client load, while messenger RNAs containing upstream open reading frames such as ATF4 and CHOP escape repression via delayed reinitiation, orchestrating adaptive stress transcriptome.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 7, Phosphorylation of eIF2alpha leading to global translation shutdown via eIF2B sequestration

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Translation in Prokaryotes and Eukaryotes

Which factor is phosphorylated at Ser51 during stress?

Eukaryotic initiation factor eIF2 alpha subunit undergoes regulatory phosphorylation at conserved serine 51 in N-terminal OB-fold domain by four distinct stress kinases: PERK activated by unfolded proteins in endoplasmic reticulum, PKR that senses viral double-stranded RNA, GCN2 responding to uncharged tRNAs during amino acid starvation, and HRI sensing heme deficiency and oxidative stress. Phosphorylation converts eIF2 from substrate to competitive inhibitor of its guanine exchange factor eIF2B, because affinity increases dramatically, inactivating eIF2B due to limiting concentration, thereby initiating integrated stress response and reprogramming translation.

Ref: Berg et al., Biochemistry, 9th ed., Chapter 32, eIF2alpha Ser51 phosphorylation by PERK, PKR, GCN2 kinases

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A Cell Signaling

FOXO target gene expression increases in which condition?

All of these, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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