Pericardin, a Drosophila collagen, facilitates accumulation of hemocytes at the heart.

Hematopoietic cell lineages support organismal needs by responding to positional and systemic signals that balance proliferative and differentiation events. Drosophila provides an excellent genetic model to dissect these signals, where the activity of cues in the hemolymph or substrate can be traced to determination and differentiation events of well characterized hemocyte types. Plasmatocytes in third instar larvae increase in number in response to infection and in anticipation of metamorphosis. Here we characterize hemocyte clustering, proliferation and transdifferentiation on the heart or dorsal vessel. Hemocytes accumulate on the inner foldings of the heart basement membrane, where they move with heart contraction, and are in proximity to the heart ostia and pericardial nephrocytes. The numbers of hemocytes vary, but increase transiently before pupariation, and decrease by 4 h before pupa formation. During their accumulation at the heart, plasmatocytes can proliferate and can transdifferentiate into crystal cells. Serrate expressing cells as well as lamellocyte-like, Atilla expressing ensheathing cells are associated with some, but not all hemocyte clusters. Hemocyte aggregation is enhanced by the presence of a heart specific Collagen, Pericardin, but not the associated pericardial cells. The varied and transient number of hemocytes in the pericardial compartment suggests that this is not a hematopoietic hub, but a niche supporting differentiation and rapid dispersal in response to systemic signals. • Clusters of hemocytes transiently collect in the heart ECM hours before pupariation in Drosophila. • In the absence of Pericardin, a Drosophila heart Collagen, this aggregation is greatly reduced. • Hemocyte trans-differentiation is observed in the pericardial aggregates. • Although mitosis is rare, lamellocyte-like ensheathing cells and Serrate expressing cells are observed. • Pericardial aggregation is enhanced and accelerated in response to environmental bacteria. [ABSTRACT FROM AUTHOR]