Mutant/mutation
The mutant lacks expression of PY01365, one member of the py235 gene family.
(The gene model of P. yoelii X (XNL) is shown; however, the gene has been deleted in P. yoelii YM; sequence differences exists between members of the py235 (reticulocyte binding protein) gene family between these two laboratory strains)

Protein (function)
Of the Plasmodium erythrocyte adhesion ligand families identified to date, one of the most studied is the erythrocyte binding ligand family (EBL), which includes P. falciparum erythrocyte binding antigen (EBA)-175 and the Duffy binding protein (DBP) of P. vivax and P. knowlesi, located in the apical organelles of the merozoite.

A second group of high molecular mass adhesion proteins, which was first described in the rodent malaria parasite P. yoelii as Py235 is the reticulocyte binding-like (RBL) super family, so named because of sequence homology with the reticulocyte binding protein RBP-1 and RBP-2 of P. vivax. In P. vivax, these proteins are thought to be involved in erythrocyte selection as they bind to reticulocytes but not mature erythrocytes thereby restricting P. vivax to the invasion of reticulocytes. P. falciparum contains a small group of genes coding for proteins with similarities to Py235 and PvRBP, the PfRH family. In contrast to the PvRBP and PfRH gene families, which are small, the Py235 multigene family contains at least 11 members. Analysis of the sequences on fifteen contigs identified in the P. yoelii genome database, which represent members of the Py235 gene family (and some of which are incomplete), show they have overall conserved structural elements.
The Py235 proteins have been implicated in the selection, recognition and invasion of erythrocytes. Populations of P. yoelii asexual blood stage parasites express multiple members of the py235 gene family.The member Py235EBP-1 (encoded by the single copy gene PY01365) is recognized by mAb 25.77. In both virulent and avirulent P. yoelii parasites, PY01365 is the most abundantly transcribed Py235 member.

Phenotype
The mutant showed a different (delayed) course of parasitemia in BALB/c mice and BALB/c mice showed a delayed death from infection (see further 'Additional Information).

The pehenotype of an independent mutant lacking expression of  PY01365 (RMgm-405) has been reported. The phenotype of this mutant is different from the phenotype reported in this study (see 'Additional Information' below).

Additional information
Data is presented that suggests that the disruption of PY01365 leads to the increased expression of members of Py235 that are not recognized by 25.77.

A significant percentage (35-41%) of mutant schizonts stained with mAb 25.77 confirming that the protective 25.77 antibody does not only recognize a single variant of Py235.

Quantitative RT-PCR analyses indicate that disruption of PY01365 leads to a change in the overall transcription pattern of different members of Py235.

In an independent study the phenotype has been analysed from an independent P. yoelii mutant lacking expression of PY01365 (see RMgm-405).  Host cell preference (reticulocytes, normocytes), growth/multiplication rate of asexual blood stages of this mutant was NOT different from wild type parasites. Evidence is presented that there was no compensatory significant upregulation of expression of any of the other Py235 genes in the mutant parasite. For this mutant it has been suggested that that the protein PY01185  is able to fulfill the role of PY01365 by serving as an invasion ligand.

Other mutants
RMgm-405: An independent mutant lacking expression of PY01365.