Match List-I with List-II

Choose the correct answer from the options given below:

(A)-(IV), (B)-(III), (C)-(II), (D)-(I)

The correct answer is Option (3) → (A)-(IV), (B)-(III), (C)-(II), (D)-(I)

A. Bt toxin is produced by a bacterium called Bacillus thuringiensis (Bt for short). Bt toxin gene has been cloned from the bacteria and been expressed in plants to provide resistance to insects without the need for insecticides; in effect created a bio-pesticide. Examples are Bt cotton, Bt corn, rice, tomato, potato and soyabean etc. Some strains of Bacillus thuringiensis produce proteins that kill certain insects such as lepidopterans (tobacco budworm, armyworm), coleopterans (beetles) and dipterans (flies, mosquitoes). B. thuringiensis forms protein crystals during a particular phase of their growth. These crystals contain a toxic insecticidal protein. Actually, the Bt toxin protein exist as inactive protoxins but once an insect ingest the inactive toxin, it is converted into an active form of toxin due to the alkaline pH of the gut which solubilise the crystals. The activated toxin binds to the surface of midgut epithelial cells and create pores that cause cell swelling and lysis and eventually cause death of the insect.

B. Several nematodes infect a wide variety of plants and animals including human beings. A nematode Meloidegyne incognitia infects the roots of tobacco plants which reduce the production of tobacco plants and reduces the production of tobacco. Thus, to prevent this infection a strategy is adopted known as RNA interface (RNAi) which takes place in all eukaryotic organisms as a method of cellular defence. This method involves silencing of mRNA due to complementary dsRNA molecule that binds to it and prevents the process of translation of mRNA.

C. In 1983, Eli Lilly an American company prepared two DNA sequences corresponding to A and B, chains of human insulin and introduced them in plasmids of E. coli to produce insulin chains. Chains A and B were produced separately, extracted and combined by creating disulfide bonds to form human insulin.

D. In 1990, the first clinical gene therapy was administered to a 4-year-old girl who had adenosine deaminase (ADA) deficiency, a condition essential for the proper functioning of the immune system. This deficiency arises due to the deletion of the gene responsible for producing ADA. Mutations in the ADA gene lead to a deficiency or absence of this enzyme, causing a buildup of harmful substances like deoxyadenosine, which can be toxic to lymphocytes and other cells. This can result in severe combined immunodeficiency (SCID), a condition where the body's ability to fight off infections is severely impaired.As a first step towards gene therapy, lymphocytes from the blood of the patient are grown in a culture outside the body. A functional ADA cDNA (using a retroviral vector) is then introduced into these lymphocytes, which are subsequently returned to the patient. However, as these cells are not immortal, the patient requires periodic infusion of such genetically engineered lymphocytes. However, if the gene isolate from marrow cells producing ADA is introduced into cells at early embryonic stages, it could be a permanent cure.