In sickle-cell disease, as a result of a single amino acid change, the hemoglobin tetramers associate with each other and assemble into large fibers. Based on this information alone, we can conclude that sickle-cell hemoglobin exhibits .

One of the common genetic disorders is sickle cell anemia, in which 2 recessive alleles must meet to allow for destruction and alteration in the morphology of red blood cells. This usually leads to loss of proper binding of oxygen to hemoglobin and curved, sickle-shaped erythrocytes. The mutation causing this disease occurs in the 6th codon of the HBB gene encoding the hemoglobin subunit β (β-globin), a protein, serving as an integral part of the adult hemoglobin A (HbA), which is a heterotetramer of 2 α chains and 2 β chains that is responsible for binding to the oxygen in the blood. This mutation changes a charged glutamic acid to a hydrophobic valine residue and disrupts the tertiary structure and stability of the hemoglobin molecule. Since in the field of protein intrinsic disorder, charged and polar residues are typically considered as disorder promoting, in opposite to the order-promoting non-polar hydrophobic residues, in this study we attempted to answer a question if intrinsic disorder might have a role in the pathogenesis of sickle cell anemia. To this end, several disorder predictors were utilized to evaluate the presence of intrinsically disordered regions in all subunits of human hemoglobin: α, β, δ, ε, ζ, γ1, and γ2. Then, structural analysis was completed by using the SWISS-MODEL Repository to visualize the outputs of the disorder predictors. Finally, Uniprot STRING and D2P2 were used to determine biochemical interactome and protein partners for each hemoglobin subunit along with analyzing their posttranslational modifications. All these properties were used to determine any differences between the 6 different types of subunits of hemoglobin and to correlate the mutation leading to sickle cell anemia with intrinsic disorder propensity.

Explanation:

transcription is a process in which information is rewritten. it is something our cells must do, in a more specialized and narrowly defined way. in biology, transcription is the process of copying out the dna sequence of a gene in the similar alphabet of rna. it needs to happen in the nucleus because that's where the dna is. dna is always inside the nucleus unless the cell is dividing.

transcription is the first step in gene expression, which involves copying a gene's dna sequence to make an rna molecule. transcription is performed by rna polymerases. it has three stages: initiation, elongation, and termination. rna molecules must be processed after transcription in eukaryotes.

explanation:

long version:

the protein synthesis consists two processes which are, transcription and translation. transcription takes place in the nucleus. it uses dna as a template to make an rna molecule. rna then leaves the nucleus and goes to a ribosome in the cytoplasm, where translation occurs. transcription is the first part of the central dogma of molecular biology: dna → rna. it is the transfer of genetic instructions in dna to messenger rna (mrna). during transcription, a strand of mrna is made that is complementary to a strand of dna.  

these three stages are:

  initiation: in which   is the beginning of transcription.occuring when the enzyme rna polymerase binds to a region of a gene called the promoter. this signals the dna to unwind so the enzyme can ‘‘read’’ the bases in one of the dna strands. the enzyme is now ready to make a strand of mrna with a complementary sequence of bases.

    elongation: in which is the addition of nucleotides to the mrna strand. rna polymerase reads the unwound dna strand and builds the mrna molecule, using complementary base pairs. there is a brief time during this process when the newly formed rna is bound to the unwound dna. during this process, an adenine (a) in the dna binds to an uracil (u) in the rna.

    termination: in which is the ending of transcription, and occurs when rna polymerase crosses a stop (termination) sequence in the gene. the mrna strand is complete, and it detaches from dna.

an individual’s sex (i.e., whether they are a male or female) is determined by the sex chromosomes. most people have two sex chromosomes, one that is inherited from their mother and one that is inherited from their father. typically, females have two x chromosomes (xx) and males have one x chromosome and one y chromosome (xy). conditions caused by changes (“mutations”) in genes located on the x chromosome are considered x-linked.

x-linked recessive inheritance

most x-linked conditions are recessive. this means that in a person with two x chromosomes (most females), both copies of a gene (i.e., one on each x chromosome) must have a change or mutation whereas in a person with one x chromosome (most males), only one copy of a gene must have a mutation. a female with a mutation in one copy of a gene on the x chromosome is said to be a “carrier” for an x-linked condition. a male with a mutation in a gene on the x chromosome is typically affected with the condition. because females have two copies of the x chromosome and males have only one x chromosome, x-linked recessive diseases are more common among males than females. however, x-linked recessive diseases can occur in both males and females.

for x-linked recessive disorders, an unaffected carrier mother who has a mutation in a gene on the x chromosome can transmit either the x chromosome with this mutation or a “normal” x chromosome to her children. if the father is unaffected, none of her daughters will be affected and all of her daughters will be unaffected—since they will inherit at least one normal x chromosome from their father. however, each daughter will have a 50% chance of being an unaffected carrier like her mother and a 50% chance of both x chromosomes being normal.