Chromosomal Theory of Inheritance

Evidence for Sutton Theory

Numerous pieces of proof supported Sutton’s theory. One was that reproduction involves the initial union of only two cells, egg and sperm. If Mendel’s model was appropriate, then these 2 gametes need to make equal hereditary contributions. Sperm, however, contain little cytoplasm, suggesting that the genetic material needs to live within the nuclei of the gametes.

Furthermore, while diploid individuals have two copies of each pair of homologous chromosomes, gametes have only one. This observation was consistent with Mendel’s design, in which diploid individuals have 2 copies of each heritable gene and gametes have one.

Lastly, chromosomes segregate during meiosis, and each set of homologue orients on the metaphase plate separate from every other set. There is however one issue with this theory.

If Mendelian characters are determined by genes located on the chromosomes, and if the independent selection of Mendelian traits reflects the independent number of chromosomes in meiosis, why does the variety of characters that type separately in a provided kind of organism often greatly exceed the variety of chromosome pairs the organism possesses? This has led many early scientists to have serious reservations about Sutton’s theory.

Thomas Hunt Morgan Experiment

In 1910 Thomas Hunt Morgan, studying the fruit fly, Drosophila melanogaster, identified a mutant male fly, one that differed noticeably from normal lies of the very same species its eyes were white instead of red.

Morgan crossed the mutant male to a normal female. All F1 progeny had red eyes. He then crossed red-eyed flies from F1 generation with each other. Of the 4252 F2 progeny Morgan took a look at, 782 (18%) had white eyes. Although the ratio of red eyes to white eyes in the F2 progeny was greater than 3:1, the results of the cross nonetheless provided clear proof that eye colour segregates.

However, there was something about the outcome that was weird and completely unpredicted by Mendel’s theory – all of the white-eyed F2 flies were male.

How could this result be explained?

Maybe it was difficult for a white-eyed female fly to exist; such individuals may not be feasible for some unidentified factor. To test this idea, Morgan test crossed the female F1 progeny with the initial white-eyed male. He got both white-eyed and red-eyed males and females in a 1:1:1:1 ratio, just as Mendelian theory anticipated. Hence a female might have white eyes. Why then existed no white-eyed females among the progeny of the original cross?

The solution to this puzzle involved sex. The gene causing the white eye trait in Drosophila resides only on the X chromosome. It is missing from the Y chromosome. A characteristic determined by a gene on the X chromosome is said to be a sex-linked trait. Knowing that the white eye trait is recessive to the red-eye trait, Morgan’s result was a natural effect of the Mendelian assortment of chromosomes.

Morgan’s experiment was one of the most essential in the history of genes because it presented the first clear evidence that the genes figuring out Mendelian characteristics do undoubtedly live on the chromosomes, as Sutton had proposed. The chromosome theory of inheritance, therefore, propounds that genes are located on chromosomes. The segregation of the white-eye trait has a one-to-one correspondence with the segregation of the X chromosome, to put it simply, Mendelian characteristics such as eye colour in Drosophila assort individually because chromosomes do.

DNA as Hereditary Material

The first proof of genetic nature of DNA was provided by a British microbiologist Frederick Griffith who made some unanticipated observations while experimenting with pathogenic bacteria. When he contaminated mice with a virulent strain of Streptococcus pneumoniae bacteria (then called Pneumococcus), the mice died of blood poisoning.

However, when he infected similar mice with a mutant strain of S. pneumoniae that did not have the virulent strain polysaccharide coat, the mice showed no ill effects. The coat was apparently necessary for virulence.

The regular pathogenic kind of this bacteria is described as the S type because it forms smooth colonies on a culture dish. The mutant types, which does not have an enzyme needed to synthesize the polysaccharide coat, is called the R kind because it forms rough colonies.

To identify whether the polysaccharide coat itself had a toxic effect. Griffith injected dead bacteria of the virulent S strain into the mice; the mice stayed completely healthy. As a control, he injected mice with a mix consisting of dead S bacteria of the virulent strain and live coatless R bacteria, each of which by itself did not harm the mice. Unexpectedly, the mice developed the illness signs and much of them passed away.

The blood of the dead mice was discovered to include high levels of live, virulent streptococcus type S bacteria, which had surface area proteins particular of the live (previously R) strains. In some way, the info specifying the polysaccharide coat had actually passed from the dead, virulent S bacteria to the live, coatless R bacteria in the mix, permanently changing the coatless R bacteria into the virulent S type.

Improvement is the transfer of genetic material from one cell to another and can modify the genetic comprise of the recipient cell.

The representative responsible for transforming Streptococcus went undiscovered until 1944. In a timeless series of experiments, Oswald Avery along with Colin Macleod andMaclyn McCarty characterized what they referred to as the “Transforming Principle”.

They first prepared a mixture of dead S Streptococcus and live R Streptococcus that Griffith had actually used. Then they removed as much of the protein as they could from their preparation, ultimately accomplishing 99.98% purity. Despite the elimination of nearly all the proteins, the transforming activity was not minimized.

Additionally, the properties of the transforming principle looked like those of DNA. The protein absorbing enzymes or RNA absorbing enzymes did not affect the transforming principles activity, however, the DNA absorbing enzyme DNase ruined all the transforming activity.

Extra evidence supporting Avery’s conclusion was provided in 1952 by Alfred Hershey and Martha Chase who explore bacteriophages T2. In some experiments, they identified viruses with radioisotope 32P, which was included in the recently synthesized DNA of grooving phage.

In other experiments, the viruses were grown on a medium including 35S, an isotope of sulphur that is incorporated into the amino acids of newly manufactured protein coats.

After the labeled viruses were allowed to contaminate bacteria, the bacterial cells were agitated strongly to remove the protein coats of the infecting viruses from the surface areas of the bacteria. This procedure eliminated nearly all of the 35S label from the bacteria. Nevertheless, the 32P label had transferred to the interior of the bacteria and was discovered in viruses consequently released from the infected bacteria. Hence, the genetic info injected into the bacteria that specified the new generation of viruses was DNA and not protein.

 

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