Unlike many plant miRNA targets, which are almost completely complementary in open reading frames (ORFs) [ 18], the binding between animal miRNAs and their target sites has incomplete complementarity in base-pairing, and binding sites can be found in 3' UTRs, 5' UTRs and coding regions of target genes [ 19- 21].
First, animal miRNAs have been found to mediate mRNA degradation even when the target sites have incomplete complementarity to them [20] [22].
In addition, for most targets, 5′ dominant complementarity to the seed region or incomplete complementarity to 5′ and 3′ (3′UTR compensatory) occurs, resulting in translational suppression [11,12].
Duplex RNA were designed to have incomplete complementarity with the 3'UTR sequences of both target genes.
Since miRNAs usually pair with incomplete complementarity to their targets, bioinformatic approaches to identify targets are limited and functional analysis is required to prove mRNA:miRNA interactions.
In the mammalian cytoplasmic context, miRNAs attach to their target with incomplete complementarity in association with cellular proteins commonly called the RNA-Induced Silencing Complex (RISC).
The former usually are located in intergenic regions and share only poor and incomplete complementarity with target sequences, which complicates computational target predictions.
However, it has been well reported that small RNAs can be effective against single and multiple target mRNAs with incomplete complementarity [34], [35].
If the miRNA binds with incomplete complementarity then it causes translational repression of the mRNA.
In contrast, in humans, miRNAs bind to mRNA targets with incomplete complementarity, which results in mRNA destabilisation and translational inhibition.
However, for a long time it has been believed that miRNA targeting in plants requires almost complete complementarity while in animal it is incomplete complementarity where seed regions play the critical role in binding and subsequent targeting [ 1, 2].
