We discuss the mechanisms of de novo palindrome formation and palindromic amplification in cancer cells, as well as possible roles preexisting DNA palindromes and short inverted repeats might have in these processes. Palindromic amplification of genes is one of the hallmarks of cancer cells and is often linked to poor treatment prognosis. In Section 3, we focus on the role DNA palindromes play in carcinogenesis. We explain why palindromes are recombinogenic and what is the current understanding of molecular mechanisms underlying palindrome recombinogenicity in eukaryotic cells.

First, in Section 2 of this review, we explore the recombinogenic nature of palindromic sequences.

As a response to the breakage (double-strand break-DSB) in DNA, the cell employs various repair mechanisms which can ultimately result in genetic rearrangements. The architecture of the genome is complex and wondrous, with sequences that play various important roles, but also those, such as DNA palindromes, that create fragile sites (i.e., sites prone to potentially lethal chromosome breakage), thus endangering genome stability. Furthermore, we overview the data on known palindromic sequences in the human genome and efforts to estimate their number and distribution, as well as underlying mechanisms of genetic rearrangements specific palindromic sequences cause.Īs the exploration of various genomes, including our own, moves forward thanks to ever more advanced and more easily available techniques, it is becoming clear that the genome is much more than the assembly of genes. Here, we bring an overview of current understanding and knowledge on molecular mechanisms of palindrome recombinogenicity and discuss possible implications of DNA palindromes in carcinogenesis. Given their recombinogenic nature, it is not surprising that palindromes in the human genome are involved in genetic rearrangements in cancer cells as well as other known recurrent translocations and deletions associated with certain syndromes in humans. The ability of certain palindromes to initiate genetic recombination lies in their ability to form secondary structures in DNA which can cause replication stalling and double-strand breaks. However, many palindromes are known as fragile sites in the genome, sites prone to chromosome breakage which can lead to various genetic rearrangements or even cell death. Certain palindromes have important biological functions as parts of various cis-acting elements and protein binding sites. 2012.A palindrome in DNA consists of two closely spaced or adjacent inverted repeats. When the complementary strand is read backwards, the sequence is 5’-GGATCC-3’ which is identical to the first one, making it a palindromic sequence. This is the sequence where the restriction endonuclease, BamHI, binds to and cleaves at a specific cleavage site. An example of a palindromic sequence is 5’-GGATCC-3’, which has a complementary strand, 3’-CCTAGG-5’. So if a sequence is palindromic, the nucleotide sequence of one strand would be the same as its reverse complementary strand. The pairing of nucleotides within the DNA double-helix is complementary which consist of Adenine (A) pairing with either Thymine (T) in DNA or Uracil (U) in RNA, while Cytosine (C) pairs with Guanine (G). Recognition sites of many restriction enzymes are palindromic. The sequence is the same when one strand is read left to right and the other strand is read right to left. A DNA sequence whose 5'-to-3' sequence is identical on each DNA strand.

Palindromic sequence with pallendrome