Evolution of Infectious Agents: Genes and Functions

Mutations are heritable changes in the genome that do not result in genotypic variation.

Successful mutations are those that do not impart any selective advantage to the organism.

Directed change is the only way mutations can arise according to Luria and Delbrück.

The frequency of DNA replication errors in wild type E. coli is approximately $1 imes 10^{-3}$ per genome per generation.

Bacterial genetics is highly predictable and follows a linear pattern similar to a small town.

Horizontal gene transfer only occurs between bacteria and their host organisms.

During base substitution, transition occurs when a purine switches to a pyrimidine.

In frameshift mutations, the wild type reading frame remains the same even if one or more bases are inserted or deleted.

The presence of stop codons like UAA, UAG, and UGA in DNA sequences can lead to nonsense mutations.

A synonymous mutation results in changing the amino acid sequence of a protein.

Genetic rearrangements involve changes in the sequence of nucleotides within a gene.

Pathogens always cause disease by growing and colonizing in the host organism.

In evolution, new genes can only arise de novo without any relation to existing genes.

Horizontal gene transfer is an intrinsic mechanism for the emergence of new genes in bacteria.

Gene duplication can lead to the emergence of new functions in proteins due to mutations in the extra copy.

Point mutations have a high likelihood of directly leading to the emergence of new functions.

Gene gain and gene loss are part of the process of genome reduction in bacteria.

Mutation during non-functionality model suggests that new genes can emerge when an existing gene is duplicated during non-functionality.