Cis-natural antisense transcript

[3] Current evidence has suggested a variety of regulatory roles for NATs, such as RNA interference (RNAi), alternative splicing, genomic imprinting, and X-chromosome inactivation.

[5] Trans-NATs are transcribed from a different location than their targets and usually have complementarity to multiple transcripts with some mismatches.

[6] Cis-natural antisense transcripts (cis-NATs) on the other hand are transcribed from the same genomic locus as their target but from the opposite DNA strand and form perfect pairs.

Identification of NATs in whole genomes is possible due to the large collection of sequence data available from multiple organisms.

In silico methods for detecting NATs suffer from several shortcomings depending on the source of sequence information.

[1] Combinations of the different sequence sources attempts to maximize coverage as well as maintain integrity in the data.

The first model attributes that base pairing between the cis-NAT and its complementary transcript result in a knockdown of mRNA expression.

RNA polymerases will then begin transcribing the gene at the transcription initiation site laying down nucleotides in a 5' to 3' direction.

A flurry of interest in gene regulatory networks has been sparked by the advent of sequenced genomes of multiple organisms.

[12] Evolutionary reasons for utilizing RNA for regulation of genes may be that it is less costly and faster than synthesizing proteins not needed by the cell.

[4] It is thought that in malignant cancer cells with activated transposable elements creates a large amount of transcriptional noise.

Figure 1: Orientations of cis-NATs within the genome
Transcription collision model for expression inhibition
Figure 3: Aberrant transcription of antisense transcripts can result in inhibition of oncogenes and allow cell to continue past cell cycle check points. Putative new oncogenes and tumor suppressor genes can be found by looking for upregulated antisense transcripts in cancer cells.