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#cAMP

21 public questions tagged with this topic.

Dictyostelium

High extracellular cAMP induces:

High ambient extracellular cAMP acts as positional cue favoring prespore differentiation through sustained protein kinase A activation. At millimolar levels, cAMP saturates desensitization mechanisms, maintaining intracellular messenger elevated, inducing transcription of prespore-specific genes encoding spore coat proteins while repressing prestalk markers. Low-density monolayer experiments show cAMP plus conditioned medium induces prespore markers, whereas DIF-1 alone induces prestalk. High cAMP therefore mirrors posterior slug environment where prespore cells reside. Prestalk formation prefers low cAMP together with DIF-1, vegetative growth requires folate, slug dispersal demands low cAMP oscillations, highlighting dosage-dependent fate specification mechanism.

Ref: Methods in Molecular Biology, Prespore induction by high cAMP - SP70 expression and PKA signaling mechanism.

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Dictyostelium

cAMP degradation mediated by:

Temporal shaping of extracellular cAMP waves depends on regulated degradation preventing uniform saturation. Secreted phosphodiesterase PdsA hydrolyzes cAMP to AMP in extracellular medium, creating troughs between pulses that allow receptor resensitization and directional sensing. PdsA is expressed during aggregation from cAMP-inducible promoter, membrane-associated, and inhibited by specific inhibitor PdiA. RegA degrades intracellular cAMP, ACA synthesizes cAMP, PiaA couples TOR complex 2 to ACA activation. Without PdsA, cAMP accumulates uniformly, abolishing gradient, cells fail to aggregate. Thus PdsA functions as essential extracellular terminator sculpting pulsatile dynamics that organize thousands of cells into streams.

Ref: Journal of Cell Biology, PdsA extracellular phosphodiesterase - cAMP wave shaping and aggregation chemotaxis.

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Dictyostelium

Adenylyl cyclase in aggregation:

Among three adenylyl cyclases, ACA encoded by acaA is uniquely required for aggregation signaling. Transcribed from multiple developmental promoters, ACA produces both extracellular cAMP for chemotactic relay and intracellular cAMP for PKA-dependent gene expression. Null acaA cells cannot generate cAMP oscillations, remain unable to aggregate, and fail to express early genes despite starvation. Exogenous pulses can rescue development. ACB encoded by acrA acts later during culmination, while ACG encoded by acgA functions as osmosensor controlling spore dormancy. ACP is not a Dictyostelium cyclase isoform, making ACA definitive aggregation-specific enzyme.

Ref: PLOS ONE, ACA adenylyl cyclase as aggregation cyclase - acaA alternative promoters and signal relay function.

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Dictyostelium

cAMP receptors classified as:

cAMP receptors cAR1 through cAR4 are classical seven-transmembrane heterotrimeric G protein-coupled receptors with high homology to mammalian chemoattractant receptors. They couple to G alpha 2 and G beta-gamma complexes activating multiple effectors including adenylyl cyclase, phospholipase C, PI3K, and MAPK, coordinating chemotaxis and gene expression. They are not ligand-gated ion channels, receptor tyrosine kinases that autophosphorylate, or nuclear hormone receptors residing intracellularly. cAR1 possesses highest affinity, rapidly desensitizes, and establishes oscillatory dynamics essential for wave propagation. Gene disruption of cAR1 abolishes aggregation and chemotactic streaming during starvation.

Ref: NCBI Gene, Dictyostelium cAR1 as GPCR - seven transmembrane and heterotrimeric G protein chemotaxis signaling.

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Dictyostelium

cAMP production regulated by:

Biosynthesis of cAMP from ATP is catalyzed by adenylyl cyclases encoded by acaA, acrA, and acgA genes expressed at distinct stages. ACA, a twelve-transmembrane protein, dominates early aggregation, activated downstream of cAR1, heterotrimeric G proteins, and cytosolic regulator CRAC. It generates both intracellular second messenger for protein kinase A and extracellular signal for relay. Phosphatases remove phosphate groups, while lyases and esterases perform unrelated cleavages. Later ACA activity declines, replaced by ACB during culmination and ACG during spore dormancy, each regulated by developmental promoters and environmental cues like osmolarity and ligand binding.

Ref: Kessin, Dictyostelium: Evolution, Cell Biology, Chapter 4: Adenylyl cyclases ACA, ACB, ACG regulation.

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Dictyostelium

Signaling molecule guiding Dictyostelium aggregation:

Aggregation centers broadcast pulsatile 3',5'-cyclic AMP, the universal chemoattractant for Dictyostelium. Starving cells relay cAMP outward as spiral or concentric waves detectable by dark-field optics. Neighbors sense increasing concentration via high-affinity G protein-coupled cAR1 receptors that activate adenylyl cyclase ACA, producing further cAMP. This excitable relay generates directional movement up gradient. Calcium ions, ATP, or ADP do not elicit chemotaxis in this species. Periodic cAMP secretion every six minutes arises from adaptation of receptor and degradation by extracellular phosphodiesterase PdsA, ensuring wave propagation over centimeter-scale territories.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 22: cAMP oscillations, cAR1 GPCR and PdsA phosphodiesterase relay.

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Fertilization in mammals-lll

High extracellular cAMP induces in Dictyostelium:

Dictyostelium discoideum aggregation forms multicellular slug that later differentiates into prestalk and prespore zones. Extracellular cAMP serves dual role chemotactic signal and morphogen; within slug tip, high cAMP concentration suppresses prestalk differentiation while promoting prespore fate via activation of cAMP-dependent protein kinase and transcription factors. Prestalk cells preferentially arise at anterior where low extracellular cAMP and higher DIF-1 prevail. Experimental addition of high exogenous cAMP converts cells toward prespore lineage expressing spore coat proteins. Thus high extracellular cAMP milieu, not low, drives prespore formation, contrasting with low cAMP favoring stalk during culmination and ensuring proper proportioning.

Ref: Shaulsky et al., Nature 1996 & Saran et al., Development 2002: Dictyostelium cAMP signaling and prespore prestalk differentiation.

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Gene regulation in Prokaryotes

CAP-cAMP complex binds when

Catabolite repression couples glucose availability to cyclic AMP synthesis via adenylate cyclase. When glucose transport is low, EIIA phosphorylated activates cyclase, raising cAMP levels. Cyclic AMP binds catabolite activator protein CAP, inducing conformational shift allowing dimerization and DNA recognition. The CAP-cAMP complex binds conserved sites near catabolite-sensitive promoters including lac, ara, gal, facilitating RNA polymerase recruitment through alpha-CTD contact. When glucose abundant, cAMP falls, CAP remains inactive, transcription of alternative sugar operons reduced. Thus CAP-cAMP binding specifically signals carbon starvation and glucose limitation, coordinating hierarchical sugar utilization for energy efficiency.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 8: Bacterial Transcription Control and CAP-cAMP

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Lac Operon

CAP becomes active when bound to

Catabolite activator protein exists in equilibrium between inactive and active conformations controlled by small molecule ligand binding allosterically. Each protomer of the homodimer contains N-terminal cyclic-nucleotide-binding domain that specifically accommodates cyclic AMP in anti conformation. cAMP binding triggers hinge repositioning and ordering of C-terminal helix-turn-helix DNA recognition motif able to bind consensus TGTGA-N6-TCACA half sites with high affinity. Resulting CRP-cAMP-DNA ternary complex bends DNA and activates transcription initiation. ATP and GTP do not serve as allosteric effectors for this protein, glucose actually lowers cAMP indirectly via PTS-mediated regulation of adenylate cyclase enzymatic activity controlling synthesis.

Ref: NCBI Biochemistry - CAP becomes active when bound to cAMP allosteric activation; Alberts Chapter 7 catabolite repression

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A Cell Signaling

Addition of cAMP in PKA knockdown cells causes:

No transcriptional change, 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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A Cell Signaling

Which hormone uses cAMP as second messenger?

Calcitonin, 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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Cell Signaling GPCR Pathways - I

Second messenger in olfactory signaling is

cAMP, 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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