Phosphatidylserine Receptor Is Required for Clearance of Apoptotic Cells

  title={Phosphatidylserine Receptor Is Required for Clearance of Apoptotic Cells},
  author={Ming O. Li and Matthew R Sarkisian and Wajahat Zafar Mehal and Pasko Rakic and Richard A. Flavell},
  pages={1560 - 1563}
Cells undergoing apoptosis during development are removed by phagocytes, but the underlying mechanisms of this process are not fully understood. Phagocytes lacking the phosphatidylserine receptor (PSR) were defective in removing apoptotic cells. Consequently, in PSR-deficient mice, dead cells accumulated in the lung and brain, causing abnormal development and leading to neonatal lethality. A fraction of PSR knockout mice manifested a hyperplasic brain phenotype resembling that of mice deficient… 

The phosphatidylserine receptor has essential functions during embryogenesis but not in apoptotic cell removal

Ptdsr is essential for the development and differentiation of multiple organs during embryogenesis but not for apoptotic cell removal, and may have a novel, unexpected developmental function as an important differentiation-promoting gene, contradict the current view that the phosphatidylserine receptor primarily functions in apoptosis.

Changing story of the receptor for phosphatidylserine‐dependent clearance of apoptotic cells

This review summarizes the current status of research on the PSR protein and indicates that it has a JumonjiC domain, and the molecular features characteristic of Fe(II)‐dependent and 2‐oxoglutarate‐dependent oxygenases.

The Presumptive Phosphatidylserine Receptor Is Dispensable for Innate Anti-inflammatory Recognition and Clearance of Apoptotic Cells*

It is concluded that PSR is not involved generally in either specific innate recognition or engulfment of apoptotic cells, and does not play a role in pro-inflammatory transcription or in the anti-inflammatory modulation of that transcriptional response triggered by apoptosis.

Phosphatidylserine receptor is required for the engulfment of dead apoptotic cells and for normal embryonic development in zebrafish

Results are consistent with aPSR-dependent system in zebrafish embryos that engulfs apoptotic cells mediated by PSR-phagocytes during development, with the system assuming an important role in the normal development of tissues such as the brain, heart, notochord and somite.

The Drosophila homolog of the putative phosphatidylserine receptor functions to inhibit apoptosis

Exposure of phosphatidylserine is a conserved feature of apoptotic cells and is thought to act as a signal for engulfment of the cell corpse, but it is surprised to find that overexpression of d PSR protects from apoptosis, while loss of dPSR enhances apoptosis in the developing eye.

Phosphatidylserine receptor and apoptosis: consequences of a non-ingested meal

  • M. Botto
  • Biology
    Arthritis research & therapy
  • 2004
Some of the arguments that underpin the importance of these clearance mechanisms are re-examine in light of recent observations from an animal model that lacks the receptor specific for phosphatidylserine.

Identification of Tim4 as a phosphatidylserine receptor

Results indicate that Tim4 and Tim1 are phosphatidylserine receptors for the engulfment of apoptotic cells, and may also be involved in intercellular signalling in which exosomes are involved.

An Apoptotic 'Eat Me' Signal: Phosphatidylserine Exposure.

Draper-mediated and Phosphatidylserine-independent Phagocytosis of Apoptotic Cells by Drosophila Hemocytes/Macrophages*

The mechanism of phagocytic elimination of dying cells in Drosophila is poorly understood. This study was undertaken to examine the recognition and engulfment of apoptotic cells by Drosophila



Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl

It is shown that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death.

Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice

CPP32 is shown to play a critical role during morphogenetic cell death in the mammalian brain during embryonic day 12, resulting in a variety of hyperplasias and disorganized cell deployment.

The phagocytosis of apoptotic cells.

The combined investigation of nematode and mammalian models has allowed, in recent years, a fast progression in the field; however, effort is still required to dissect thoroughly the molecular rules orchestrating engulfment.

Phagocytosis and clearance of apoptotic cells is mediated by MER

The Mer receptor tyrosine kinase seems to be critical for the engulfment and efficient clearance of apoptotic cells, which has implications for inflammation and autoimmune diseases such as systemic lupus erythematosus.

Identification of a factor that links apoptotic cells to phagocytes

Results indicate that milk fat globule-EGF-factor 8 secreted from activated macrophages binds to apoptotic cells, and brings them to phagocytes for engulfment.