Amino acid replacement: C80Y. Nucleotide substitution: G174A. The mutation is within the PGRP domain.
G11562211A
G174A
C80Y | PGRP-SA-PA; C80Y | PGRP-SA-PB
C80Y
PGRP-SAseml mutant flies show reduced survival rate upon infection with either Staphylococcus aureus or Streptococcus pyogenes compared to wild-type.
PGRP-SAseml mutant flies show significantly decreased survival rate upon infection with the Staphylococcus aureus strain COL and unlike wild-type flies is strongly susceptible even to infection with the strain COL MIN, which shows attenuated virulence and is unable to grow in healthy wild-type flies but grows normally in the immunocompromised PGRP-SAseml mutants.
PGRP-SAseml mutant flies show an increased susceptibility to challenge by Staphylococcus aureus or Enterococcus faecalis compared to wild type flies.
Mutant flies are susceptible to S. aureus infection compared to wild-type adults.
Hemolymph clots from PGRP-SAseml third instar larvae show normal melanization.
PGRP-SAseml mutant adults phagocytose E.coli normally, but phagocytosis of S.aureus is reduced.
Mutant flies show similar survival rates as control flies following natural infection (feeding with contaminated food) with either "Ecc-15" (P.carotovorum.carotovorum), S.cerevisiae or M.luteus.
PGRP-SAseml flies show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).
Mutant flies show reduced survival compared to wild-type controls after infection with either S. pyogenes or S. aureus.
PGRP-SAseml flies are susceptible to infection by Gram-positive bacteria (E.faecalis, S.aureus or M.luteus). PGRP-SAseml flies are resistant to fungal infection (A.fumigatus or B.bassiana) and to infection by Gram-negative bacteria (P.carotovorum.carotovorum).
Mutants are highly susceptible to Gram-positive infection, but are resistant as wild-type to fungal and Gram-negative bacterial infection.
PGRP-SAseml has abnormal immune response | adult stage phenotype, non-enhanceable by PGRP-SDsk1
PGRP-SAseml has abnormal immune response phenotype, non-enhanceable by Scer\GAL4da.G32/GNBP1RNAi.UAS
PGRP-SAseml has abnormal immune response phenotype, non-enhanceable by GNBP1e03371
PGRP-SAseml has abnormal immune response phenotype, non-enhanceable by nec1/nec2
PGRP-SAseml has abnormal immune response phenotype, non-suppressible by nec1/nec2
PGRP-SAseml is a non-enhancer of abnormal immune response phenotype of GNBP1RNAi.UAS, Scer\GAL4da.G32
PGRP-SAseml is a non-enhancer of abnormal immune response phenotype of GNBP1e03371
PGRP-SAseml is a non-enhancer of melanotic necrosis phenotype of nec1/nec2
PGRP-SAseml is a non-suppressor of melanotic necrosis phenotype of nec1/nec2
PGRP-SAseml is a non-enhancer of adult epidermis phenotype of nec1/nec2
PGRP-SAseml is a non-suppressor of adult tracheal system phenotype of Scer\GAL4btl.PS, Spn77BaRNAi.WIZ.UAS
PGRP-SAseml is a non-suppressor of adult epidermis phenotype of nec1/nec2
The reduced survival rate of PGRP-SAseml mutant adults upon infection with either Staphylococcus aureus or Streptococcus pyogenes is not worsened further by combination with PGRP-SDsk1.
The melanisation of the adult tracheal system caused by expression of Spn77BadsRNA.WIZ.Scer\UAS under the control of Scer\GAL4btl.PS is not suppressed by PGRP-SAseml.
PGRP-SDΔ3 PGRP-SAseml and GNBP1e03371 PGRP-SAseml double mutant flies are extremely susceptible to S. aureus infection compared to wild-type adults.
Flies expressing GNBP1dsRNA.Scer\UAS under the control of Scer\GAL4da.G32 in a PGRP-SAseml background show the same degree of susceptibility to M.luteus as either PGRP-SAseml single mutant flies or flies expressing GNBP1dsRNA.Scer\UAS under the control of Scer\GAL4da.G32 in a wild-type background.
PGRP-SAseml is rescued by PGRP-SAUAS.cMa/Scer\GAL4da.G32
Etymology: The mutation semmelweis is named after Ignaz Philipp Semmelweis, a Hungarian physician who was a pioneer in the field of antiseptic treatments and discovered the cause of puerperal fever.