In 1979, bones found outside Ekaterinburg, Russia, were shown to be those of Tsar Nicholas and his family, who were executed in 1918 by a Bolshevik firing squad in the Russian Revolution . To prove that the skeletons were those of the royal family, mtDNA was extracted from the bone samples, amplified by PCR, and compared with mtDNA from living relatives of the tsar’s family. Q. Mitochondrial DNA from which living relatives would provide useful information for verifying that the skeletons were those of the royal family?

Determine which statements could be used as evidence to support the argument that "DNA influences the proteins that are made" and which statements are just facts. [Select all that apply.] The HBB gene that makes beta-globin has several abnormal alleles, including HbS, HbC, and HbE. Sickle cell disease has been successfully treated using bone marrow transplantation in children and adults. The symptoms of sickle cell anemia may not appear in individuals who only carry one HbS allele, but are always apparent when both alleles are HbS. If oxygen is removed from red blood cells made by two HbS alleles, the cell will form a sickle shape.

Payne, B. A. et al. (2013) present evidence that a low level of heteroplasmic mtDNA exists in all tested healthy individuals. (a) What are two likely sources of such heteroplasmy? (b) What genetic conditions within a given mitochondrion are likely to contribute to such a variable pool of mitochondria?

which of the following statements about genome-wide association studies (GWAS) is correct? A) involves scanning the genomes of thousands of unrelated individuals with a particular mutation and comparing them with the genomes of individuals who do not have the mutation. B) involves scanning the genomes of thousands of unrelated individuals with a particular disease and comparing them with the genomes of individuals who do not have the disease C) attempt to identify genes that influence mutation risk D) attempt to identify genes that influence disease risk E) involves scanning the genomes of thousands of unrelated individuals with a particular disease and comparing them with the genomes of individuals who do not have the disease and GWAS attempt to identify genes that influence disease risk