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ATG8 is one of the critical genes that participate in several essential autophagic steps. The expression of ATG8 must be exquisitely regulated to avoid physiological disorder and even cell death. However, the mechanisms of regulating ATG8 expression remain to be fully uncovered. In this investigation, we found that Dicer homologs in Cryptococcus neoformans could activate the expression of ATG8 independent of RNAi. Deletion of two Dicer homologs (DCR1 and DCR2) from C. neoformans, especially DCR2, led to significantly reduced Atg8 protein level, but deletion of other RNAi components did not result in the same phenotype. The autophagic flux, the numbers of autophagic bodies and the tolerance to glucose starvation of dcr2∆ were also significantly reduced. Further investigation showed that Dcr2 activates the expression of ATG8 through the promoter region, not the Open Reading Frame or 3′ Untranslated Region. We also found that a similar phenomenon exists in mammalian cells, as DCR1 instead of AGO2 knockdown also reduced the expression of LC3, indicating that this mechanism may be conservative in eukaryotic cells. Therefore, a novel transcription activation mechanism was revealed in this paper.

Dicer promotes Atg8 expression through RNAi independent mechanism in Cryptococcus neoformans