Blood system formation in the urochordate Ciona intestinalis requires the variable receptor vCRL1

Mol Biol Evol. 2012 Oct;29(10):3081-93. doi: 10.1093/molbev/mss120. Epub 2012 Apr 18.

Abstract

Adaptive immune systems are present only in vertebrates. How do all the remaining animals withstand continuous attacks of permanently evolving pathogens? Even in the absence of adaptive immunity, every organism must be able to unambiguously distinguish "self" cells from any imaginable "nonself." Here, we analyzed the function of highly polymorphic gene vCRL1, which is expressed in follicle and blood cells of Ciona intestinalis, pointing to possible recognition roles either during fertilization or in immune reactions. By using segregation analysis, we demonstrate that vCRL1 locus is not involved in the control of self-sterility. Interestingly, genetic knockdown of vCRL1 in all tissues or specifically in hemocytes results in a drastic developmental arrest during metamorphosis exactly when blood system formation in Ciona normally occurs. Our data demonstrate that vCRL1 gene might be essential for the establishment of a functional blood system in Ciona. Presumably, presence of the vCRL1 receptor on the surface of blood cells renders them as self, whereas any cell lacking it is referred to as nonself and will be consequently destroyed. We propose that individual-specific receptor vCRL1 might be utilized to facilitate somatic self/nonself discrimination.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Animals
  • Cell Differentiation / genetics
  • Cell Lineage / genetics
  • Cell Membrane / metabolism
  • Ciona intestinalis / metabolism*
  • Crosses, Genetic
  • Female
  • Fertilization / genetics
  • Gene Knockdown Techniques
  • Genetic Loci / genetics
  • Genotype
  • Hemocytes / cytology
  • Hemocytes / metabolism*
  • Infertility / genetics
  • Male
  • Metamorphosis, Biological / genetics
  • Models, Biological
  • Molecular Sequence Data
  • Oocytes / cytology
  • Oocytes / metabolism
  • Phenotype
  • Polymorphism, Genetic*
  • Protein Transport
  • Receptors, Cell Surface / metabolism*

Substances

  • Receptors, Cell Surface

Associated data

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