A team of international researchers has studied autophagy induction in 40 unicellular parasitic species that could help identify novel therapeutic targets in patients suffering from colon cancer or inflammatory bowel disease (IBD).
Autophagy is a highly conserved lysosome-mediated self-degradation process, involved in survival during starvation in eukaryotic cells and also in several cellular processes, such as stress-response, protein metabolism, differentiation and aging.
This is an important process that allows intracellular pathogenic clearance, and its malfunction can lead to IBD as well as cancer progression.
Furthermore, autophagy is also important for life-cycle transitions in parasites such as Trypanosoma and Plasmodium, involved in sleeping sickness and malaria, respectively. Nevertheless, studies have yet to show how autophagy is induced in these parasites.
In this study, entitled “Starvation-response may not involve Atg1-dependent autophagy induction in non-unikont parasites” and published in Nature’s Scientific Reports, researchers used a bioinformatics approach, scanning the genomes of 40 unicellular protists parasites to examine the presence of Atg1/ULK1-like autophagy inducing complex, the primary complex inducing autophagy that receives signals of cellular nutrient status in response to nutrient depletion. However, no coding gene could be detected, demonstrating that in these parasites, autophagy is probably not dependent on an Atg1-like protein kinase system. The data appears to complement previous studies showing that ATG genes in the same organisms have different expression patterns throughout their life cycles, leading researchers to hypothesize an autophagy regulation at the post-transcriptional level.
In an interview to The Genome Analysis Center (TGAC), Dr. Tamás Korcsmáros, the TGAC-IFR Computational Biology Fellow stated, “We’re very happy that this bioinformatics study is published in such a key journal. With a detailed sequence analysis we showed that potential Atg1/ULK1 orthologs presented in many previous studies are not true counterparts of the functional autophagy inducers known in humans and many other eukaryotes. I hope our study will facilitate future experiments to understand how these dangerous parasites regulate autophagy and how we could medically use this information to overcome infectious diseases. I am particularly proud that this is my first paper since I moved to TGAC, this study is a specific example why detailed and biologically precise analysis is vital to our research, the expert knowledge and methodology at the Institute will help with the data analysis of many more genomes.”
Understanding autophagy in certain bacterial species can aid the development of therapies specifically aimed at targeting these parasites without interfering with human autophagy. Moreover, a deeper knowledge of their effect in regulating human intestinal autophagy can be the basis to identify prognosis markers for IBD and colon cancer.
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