10 public questions tagged with this topic.
The Genetic Engineering Approval Committee (GEAC) regulates the use, approval, and safety of genetically modified organisms in India. This follows from NCERT principle where the relation explains the outcome clearly for students in simple steps.
Ref: NCERT Biology Textbook for Class XI and XII (Zoology section), Chapter: Biology - Zoology portion covering relevant system and function.
The Genetic Engineering Approval Committee (GEAC) is responsible for regulating the use, approval, and safety of genetically modified organisms in India.
Ref: NCERT Biology Textbook for Class XI and XII (Zoology section), Chapter: Biology - Zoology portion covering relevant system and function.
The Genetic Engineering Approval Committee (GEAC) regulates the use, approval, and safety of genetically modified organisms (GMOs) in India. This follows from latest NCERT 2026-27 principle explaining the concept clearly for NEET students in simple steps as per rationalized syllabus.
Ref: NCERT Biology Textbook - Latest Edition for Academic Session 2026-27 (Zoology section, Rationalized Textbook for Class XI and XII), Chapter: Biology - Zoology portion (Latest NCERT Textbooks for Academic Session 2026-27 - Rationalized Edition for Class XI and XII), Topic: Structural organization, physiology, human health and related concepts as per latest syllabus.
Coordinated muscle contraction depends on interplay between chemical fuel and regulatory ion signals ensuring contraction only when needed. ATP provides both detach signal and energy currency: ATP binding to myosin head after power stroke dissociates rigor cross bridge, while its hydrolysis to ADP Pi stores elastic energy in lever arm for next stroke, and Pi plus ADP release execute mechanical work. Without ATP muscle enters rigor state as observed in cadaveric stiffness. Calcium provides temporal switch: at rest sarcoplasmic reticulum SERCA maintains cytosolic calcium about 100 nM insufficient for troponin C binding keeping tropomyosin blocked and myosin light chain kinase inactive. In striated excitation opens ryanodine receptors raising calcium tenfold unlocking thin filament. In smooth calcium calmodulin activates myosin light chain kinase phosphorylating regulatory light chains increasing actin activated ATPase. Dynein is microtubule minus end motor unrelated to actin myosin regulation. Hence availability of ATP determines whether cycles can turn while calcium determines whether they are permitted to start linking excitation to contraction.
Ref: Gordon et al., Physiol Rev 2000; Alberts Chapter 16 – Regulation of actin-myosin by ATP and Ca2+ availability.
Smooth muscle contraction lacks troponin based thin filament system found in skeletal muscle, so regulatory control migrates to the myosin itself and its energy metabolism. In resting smooth muscle myosin II molecule folded into inactive 10S conformation with low actin activated ATPase activity and sequestered heads. Elevation of cytosolic calcium from 100 nM to near 1 micromolar via L type calcium channel influx and IP3 mediated sarcoplasmic release promotes formation of calcium calmodulin complexes. These activate myosin light chain kinase which phosphorylates serine 19 of the 20 kDa regulatory light chain on each head. Phosphorylation unfolds myosin to extended 6S form and dramatically enhances cross bridge cycling. Each cycle still relies on ATP hydrolysis: ATP binding dissociates rigor actomyosin, hydrolysis to ADP Pi cocks lever arm into pre power stroke state, Pi release drives force generating swing, ADP release resets. Thus ATP turnover supplies mechanical energy while phosphorylation gates whether turnover can occur, integrating calcium signaling with energy metabolism for tonic force maintenance and latch state characteristic of visceral smooth muscle physiology.
Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 16: Smooth muscle myosin regulation by MLCK phosphorylation and ATPase cycle.
The juxtaglomerular apparatus (JGA) regulates GFR by releasing renin, which activates the renin-angiotensin system to control blood pressure.
Ref: NCERT Class 11 Biology Chapter 16: Excretory Products and their Elimination Urine Formation - Glomerular Filtration
Ferritin mRNAs contain iron responsive element IRE conserved hairpin in 5' UTR regulating translation via iron regulatory proteins IRP1 and IRP2. Low iron allows IRP binding blocking 43S scanning and 60S joining repressing synthesis. IRP1 holds Fe-S cluster converting to aconitase when iron sufficient; IRP2 degraded via FBXL5 sensing iron. High iron causes IRP dissociation permitting ferritin production storing iron in mineral core preventing Fenton reactions generating reactive oxygen species. This translational control complements transferrin receptor regulation via 3' UTR IREs stabilizing transcript when iron scarce, coordinating iron uptake, storage, and utilization balancing cellular needs.
Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 7: Iron Regulation of Ferritin Translation via IRE-IRP
enzyme inactivation, 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)
