Molecular traces of Drosophila hemocytes reveal transcriptomic conservation with vertebrate myeloid cells

PLoS Genet. 2023 Dec 19;19(12):e1011077. doi: 10.1371/journal.pgen.1011077. eCollection 2023 Dec.

Abstract

Drosophila hemocytes serve as the primary defense system against harmful threats, allowing the animals to thrive. Hemocytes are often compared to vertebrate innate immune system cells due to the observed functional similarities between the two. However, the similarities have primarily been established based on a limited number of genes and their functional homologies. Thus, a systematic analysis using transcriptomic data could offer novel insights into Drosophila hemocyte function and provide new perspectives on the evolution of the immune system. Here, we performed cross-species comparative analyses using single-cell RNA sequencing data from Drosophila and vertebrate immune cells. We found several conserved markers for the cluster of differentiation (CD) genes in Drosophila hemocytes and validated the role of CG8501 (CD59) in phagocytosis by plasmatocytes, which function much like macrophages in vertebrates. By comparing whole transcriptome profiles in both supervised and unsupervised analyses, we showed that Drosophila hemocytes are largely homologous to vertebrate myeloid cells, especially plasmatocytes to monocytes/macrophages and prohemocyte 1 (PH1) to hematopoietic stem cells. Furthermore, a small subset of prohemocytes with hematopoietic potential displayed homology with hematopoietic progenitor populations in vertebrates. Overall, our results provide a deeper understanding of molecular conservation in the Drosophila immune system.

MeSH terms

  • Animals
  • Drosophila melanogaster / genetics
  • Drosophila* / genetics
  • Gene Expression Profiling
  • Hemocytes*
  • Larva / genetics
  • Myeloid Cells
  • Transcriptome / genetics
  • Vertebrates / genetics

Grants and funding

This work was supported by the National Research Foundation (NRF) of Korea, which is funded by the Ministry of Science & ICT (2020R1A4A1018398, 2021R1A2C3005835, 2022M3E5F1018502, and RS-2023-00207840) to J.-W.N., (2019R1A2C2006848 and RS-2023-00218602) to J.S., and (2020R1A6A3A13076391) to S.-H.Y. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.