[5] Dicer was given its name in 2001 by Stony Brook PhD student Emily Bernstein while conducting research in Gregory Hannon's lab at Cold Spring Harbor Laboratory.

Dicer's ability to generate around 22 nucleotide RNA fragments was discovered by separating it from the RISC enzyme complex after initiating the RNAi pathway with dsRNA transfection.

Subsequent experiments testing RNase III family enzymes abilities to create RNA fragments narrowed the search to Drosophila CG4792, now named Dicer.

The work was done by Ian MacRae while conducting research as a postdoctoral fellow in Jennifer Doudna's lab at the University of California, Berkeley.

These domains are important in Dicer activity regulation, dsRNA processing, and RNA interference protein factor functioning.

The distance between the PAZ and RNaseIII domains is determined by the angle of the connector helix and influences the length of the micro RNA product.

[14] Both miRNAs and siRNAs activate the RNA-induced silencing complex (RISC), which finds the complementary target mRNA sequence and cleaves the RNA using RNase.

[19] In general, RNA interference is an essential part of normal processes within organisms such as humans, and it is an area being researched as a diagnostic and therapeutic tool for cancer targets.

This observation suggested a Dicer specific role in retinal health that was independent of the RNAi pathway and thus not a function of si/miRNA generation.

These non coding strands of RNA can loop forming dsRNA structures that would be degraded by Dicer in a healthy retina.

However, with insufficient Dicer levels, the accumulation of alu RNA leads to the degeneration of RPE as a result of inflammation.

However, high dicer expression in other cancers, like prostate[23] and esophageal, has been shown to correlate with poor patient prognosis.

Additionally, miRNAs expression patterns change as a result of DNA damage caused by ionizing or ultraviolet radiation.

It is likely dicer is involved in viral immunity as viruses that infect both plant and animal cells contain proteins designed to inhibit the RNAi response.

Another potential mechanism for viral pathogenesis is the blockade of dicer as a way to inhibit cellular miRNA pathways.

[25] In Drosophila, Dicer-1 generates microRNAs (miRNAs) by processing pre-miRNA, Dicer-2 is responsible for producing small interfering RNAs (siRNAs) from long double-stranded RNA (dsRNA).

As an example, Drosophila C virus encodes for protein 1A which binds to dsRNA thus protecting it from dicer cleavage as well as RISC loading.

[16] Along with being a diagnostic tool, Dicer can be used for treating patients by injecting foreign siRNA intravenously to cause gene silencing.

[30] One of the advantages of using Dicer to produce siRNA therapeutically would be the specificity and diversity of targets it can affect compared to what is currently being used such as antibodies or small molecular inhibitors.

Rice DCL expression can be affected by biological stress conditions, including drought, salinity and cold.