24 public questions tagged with this topic.
The lac operon is an inducible operon that is activated in the presence of lactose to allow lactose metabolism.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
An inducible operon, like the lac operon, is normally off but can be activated by an inducer (e.g., lactose).
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
The lac operon is regulated by a repressor protein, which prevents transcription in the absence of lactose.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
The lac operon is activated in the presence of lactose, which inactivates the repressor and allows transcription.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
The repressor protein binds to the operator region in the lac operon to block transcription in the absence of lactose.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
The lac operon is not always active; it is only activated in the presence of lactose.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
lacA encodes beta-galactoside transacetylase, 203-amino-acid enzyme transferring acetyl group from acetyl-CoA donor to C6 hydroxyl acceptor of thiogalactosides and non-metabolizable lactose analogs. Crystallographic analysis reveals left-handed beta-helix fold assembled as trimer with active sites at subunit interfaces. Physiological role appears detoxification rather than primary catabolism: acetylation prevents accumulation of disulfide-forming thiogalactosides or other potentially toxic beta-galactosides that could irreversibly modify cellular proteins or glutathione, promoting their efflux via other transporters. Deletion mutants remain fully viable on lactose because hydrolysis by beta-galactosidase suffices, indicating auxiliary protective role rather than central catabolic requirement.
Ref: ResearchGate Lac operon GeneAct – lacA thiogalactoside transacetylase involved in cellular detoxification not catabolism.
lacY gene product is lactose permease LacY, 417-residue member of major facilitator superfamily transporter folded into twelve transmembrane alpha helices forming central hydrophilic cavity accessible alternately outward and inward during cycle. It operates as galactoside-proton symporter driven entirely by proton motive force, accumulating lactose against concentration gradient for metabolic use. Protein functionality is distinct from soluble beta-galactosidase encoded by lacZ and transacetylase LacA. By concentrating intracellular beta-galactosides, LacY enables efficient generation of allolactose inducer and provides substrate for catalytic cleavage, creating autocatalytic positive feedback essential for bistable switching behavior of lac operon.
Ref: ScienceDirect Lactose Permease overview – LacY transmembrane symporter concentrates β-galactosides for hydrolysis and induction.
CAP, also called CRP, binds as homodimer to 22-base pair inverted repeat containing TGTGA-N6-TCACA consensus motif located upstream of lac promoter, typically centered at position -61.5. When glucose scarce, adenylate cyclase synthesizes second messenger cAMP that binds N-terminal effector domains of CAP, allosterically enabling C-terminal helix-turn-helix domains to specifically recognize major groove sequences. Dimer introduces approximately ninety-degree bend in DNA, contacts alpha-carboxy-terminal domain of RNA polymerase via activating region 1, stabilizes closed promoter complex, and accelerates isomerization to transcriptionally competent open complex. Upstream position avoids overlapping operator, permitting simultaneous positive and negative regulation through distinct sites.
Ref: NCBI Bookshelf – Sigma; J Bacteriol 1997: CAP-cAMP binds 61.5 bp upstream lac promoter, Type I activation.
Oc mutation alters the 21-base pair palindromic operator sequence overlapping the lac transcription start, disrupting critical base-specific contacts required for LacI repressor tetramer binding. Without stable repressor-operator interaction and tetrameric looping with auxiliary operators, promoter becomes freely accessible to sigma70 RNA polymerase holoenzyme initiating transcription. Consequently messenger synthesis of lacZYA continues even when allolactose inducer is absent. Because operator functions exclusively through cis linkage to downstream genes, the chromosome bearing Oc displays constitutive inducer-independent expression, while wild-type copy elsewhere remains regulatable, distinguishing cis-dominant constitutive from trans-recessive repressor defects.
Ref: LibreTexts 6.1.1 Use of Mutants Study lac Operon: Oc operator mutation blocks LacI binding causing constitutive.
Operator-constitutive mutations lacOc affect cis regulatory DNA element rather than diffusible trans-acting protein factor. Point mutations or small deletions in symmetric operator palindrome, especially central base pairs contacted by LacI recognition helix and critical guanine residues, drastically reduce LacI-operator binding affinity even for wild-type tetrameric repressor produced normally. Resulting transcription becomes constitutive but only for structural genes linked in cis to mutated operator on same DNA molecule, showing partial diploid cis-dominance in merodiploid tests, contrasting trans effects of lacI alleles. Promoter -10/-35 elements and CAP binding site remain structurally intact and functional, isolating defect to operator regulatory function alone.
Ref: Alberts Fig 7-38 lacOc mutation affects operator; NCBI - lacOc operator constitutive cannot bind repressor cis-dominant
Super-repressor allele lacIs encodes LacI protein altered specifically in inducer binding pocket via substitutions that block allolactose or IPTG interaction yet preserve intact helix-turn-helix DNA binding domain and tetramerization interface. These mutant proteins remain tightly bound to operator even after inducer accumulation reaches high levels, rendering lac operon unresponsive to lactose signal, phenotype termed uninducible and non-inducible. Dominance over wild-type occurs in merodiploids because super-repressor occupies operator despite normal repressor induction, preventing transcription from either chromosome copy. This contrasts with lacI- constitutive deletion and wild-type inducible regulatory phenotypes distinguishing structural domain functions of LacI protein organization.
Ref: NCBI Genetics Notes - lacIs super-repressor mutation causes uninducible phenotype; Alberts lacI super-repressor class
