Amino acid replacement: ??term.
Stop codon is introduced into the PGRP-LCx isoform, resulting in a truncated protein lacking the last 107 amino acids of this isoform.
Nucleotide substitution: G?A.
G9345880A
G?A
W392term | PGRP-LC-PA; W392term | PGRP-LC-PD; W221term | PGRP-LC-PE
??term
Mapped site of nonsense mutation based on report that it removes the last 107 amino acids of isoform PGRP-LCx, which appears to correspond to annotated isoforms PGRP-LC-PA. The G to A change may occur at the second or third base of the Trp codon to give a nonsense mutation. The exact site of mutation was not specified.
Motor neurons in PGRP-LC2/+ third instar larvae show similar mEPSP (mini excitatory postsynaptic potential) and EPSP (excitatory postsynaptic potential) amplitudes and quantal content as controls.
The neuromuscular junctions of PGRP-LC2 homozygous mutant third instar larvae present small but significant decreases in spontaneous miniature excitatory postsynaptic potential and in excitatory postsynaptic potential, but no significant changes in quantal content, as compared to controls.
The neuromuscular junctions of PGRP-LCΔE/PGRP-LC2 transheterozygous mutant third instar larvae present small but significant decrease in spontaneous miniature excitatory postsynaptic potential and increase in quantal content, but no significant effect in the excitatory postsynaptic potential, as compared to controls.
PGRP-LC2 heterozygosity has no significant effect on either spontaneous miniature excitatory postsynaptic potential, excitatory postsynaptic potential or quantal content of third instar larval neuromuscular junctions, as compared to controls.
The neuromuscular junction of PGRP-LC2 homozygous mutant third instar larvae shows similar overall structure to controls, with similar number of synaptic boutons, similar number and length of active zones, similar average vesicle number, similar vesicle diameter, similar average vesicle distance from the T-bar centroid.
Blood cells from mutant animals can phagocytose bacteria.