I’m sorry if it’s wrong but I think its D
<span>It is linear, because using the VSEPR theory, when you draw its lewis structure, you get two bonded pairs of electrons, which signifies a linear structure.</span>
Options for part A are as follows:
A) A mutation in the operator sequence
B) A mutation in the lac-Z gene
C) A mutation in the lac-Y gene
D) A super repressor mutation
Answer:
The correct answer:
Part a - A mutation in the operator sequence
Part b - It ensures that a cell dedicates resources to the production of enzymes involved in lactose metabolism only when lactose is available in the environment
Part C. true.
Explanation:
part a:
If there is a mutation in the operator sequence leads to prevent binding of the repressor which leads to allowing constitutive expression of the genes various conditions.
part b:
The biological role of the lac operon makes sure that the cell dedicates resources to the production of enzymes involved in lactose metabolism only when lactose is available in the environment
Part c:
RNA polymerase cannot transcribe the structural genes due to the repressor binds to the lac operator, therefore, the proper function of the lac operon is possible when the placement of the operator sequence between the promotor and the structural genes.
<span>The appendicular skeleton includes the bones of the shoulder girdle, the upper limbs, the pelvic girdle, and the lower limbs.</span>
<h2>GPCRs and RTKs</h2>
Explanation:
1) Phosphorylation of receptor can terminate signal or desensitize receptor: GPCRs because when signal persists a protein kinase receptor is activated,this further catalyse the phosphorylation of several serine residue at cytosolic phase of 7 transmembrane
Phosphorylated transmembrane recognized by arrestin protein blocks interaction between trimeric G protein and receptor thus blocks signal transduction
2) Autophosphorylation of receptor can initiate signal: RTKs because receptor dimerization activates intrinsic tyrosine kinase activity by which they phosphorylate its own tyrosine residue on cytosolic phase
3) Structure contains seven transmembrane helices: GPCRs because it consists of single polypeptide and spans the membrane 7 times hence called 7 transmembrane;it recognizes external signal and activates trimeric G protein
4) Ligand binding induces conformational change in receptor: RTKs because normally RTK exist in monomeric form in absence of any ligand molecule but when any ligand molecule binds receptor starts to dimerize
5) Receptor activation causes phosphorylation of its cytosolic subunits: RTKs because when receptor gets activates the intrinsic tyrosine kinase activity by which they phosphorylate its cytosolic subunits
6) An example is the insulin receptor: Insulin receptor is present on plasma membrane and belongs to RTK family and always exist in dimeric form
7) Transports some ligands through the membrane: Neither GPCR nor RTK;ligand gets transported through the membrane through ligand gated channel
8) An example is the epinephrine receptor: Epinephrine is an endocrine hormone produced by adrenal glands in stress condition and prepare body for fight and flight;Epinephrine uses GPCR signalling pathway by four different types of membrane receptors in different tissues
9) Activate heterotrimeric G proteins directly: Transmembrane protein of GPCR recognizes the external signal and activates G protein,activated G protein binds with effector enzyme and activate it which further produce or destroy secondary messenger that carry message from cell surface to cell interior
