Phenotypes associated with this allele

• Allele Symbol: Pglyrp1^tm1Rdz
• Allele Name: targeted mutation 1, Roman Dziarski
• Allele ID: MGI:2670590
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz	C.129S-Pglyrp1^tm1Rdz	MGI:5297111
hm2	Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz	involves: 129S5/SvEvBrd	MGI:2670595
hm3	Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz	involves: 129S5/SvEvBrd * BALB/c	MGI:5297160
cx4	Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz Pglyrp2^tm1Rdz/Pglyrp2^tm1Rdz	C.129S-Pglyrp1^tm1Rdz Pglyrp2^tm1Rdz	MGI:5297115

Genotype
MGI:5297111

hm1

• Allelic Composition: Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz
• Genetic Background: C.129S-Pglyrp1^tm1Rdz

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

immune system

increased susceptibility to induced arthritis ( J:178054 )

• arthritis that develops in mice treated with peptidoglycan or muramyl dipeptide (MDP) lasts longer than in similarly treated wild-type mice

• however, the severity and incidence of arthritis as in similarly treated wild-type mice

skeleton

increased susceptibility to induced arthritis ( J:178054 )

• arthritis that develops in mice treated with peptidoglycan or muramyl dipeptide (MDP) lasts longer than in similarly treated wild-type mice

• however, the severity and incidence of arthritis as in similarly treated wild-type mice

Genotype
MGI:2670595

hm2

• Allelic Composition: Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz
• Genetic Background: involves: 129S5/SvEvBrd

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality ( J:84680 )

• mortality of mutants is twice as high as that of wild-type mice following intraperitoneal infection with B subtilis

immune system

abnormal neutrophil physiology ( J:84680 )

• polymorphonuclear leukocytes are defective in intracellular killing and digestion of relatively non-pathogenic gram-positive bacteria

• mutant polymorphonuclear leukocytes are less effective than wild-type in generating oxidative burst in response to M luteus and B subtilis but not to S aureus or E coli

impaired granulocyte bactericidal activity ( J:84680 )

• defective in intracellular killing and digestion of relatively non-pathogenic gram-positive bacteria

increased susceptibility to bacterial infection ( J:84680 )

• increased susceptibility to intraperitoneal injection of gram-positve bacteria of low pathogenicity (B subtilis and M luteus) but not to injection of more pathogenic gram-positive (S aureus) or gram-negative bacteria (E coli) or to intravenous infection of B subtilis

increased susceptibility to bacterial infection induced morbidity/mortality ( J:84680 )

• mortality of mutants is twice as high as that of wild-type mice following intraperitoneal infection with B subtilis

hematopoietic system

abnormal neutrophil physiology ( J:84680 )

• polymorphonuclear leukocytes are defective in intracellular killing and digestion of relatively non-pathogenic gram-positive bacteria

• mutant polymorphonuclear leukocytes are less effective than wild-type in generating oxidative burst in response to M luteus and B subtilis but not to S aureus or E coli

impaired granulocyte bactericidal activity ( J:84680 )

• defective in intracellular killing and digestion of relatively non-pathogenic gram-positive bacteria

Genotype
MGI:5297160

hm3

• Allelic Composition: Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz
• Genetic Background: involves: 129S5/SvEvBrd * BALB/c

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:178053 )

• in DSS-treated mice

digestive/alimentary system

gastrointestinal hemorrhage ( J:178053 )

• severe in DSS-treated mice

abnormal intestinal epithelium morphology ( J:178053 )

• DSS-treated mice exhibit extremely severe intestinal bleeding with moderate hyperplasia of the lamina propria, thickened submucosa, loss of morphology and crypt architecture, progressive complete loss of colonic epithelial layer, decrease in goblet cells, and severe ulceration compared with similarly treated wild-type mice

abnormal intestinal mucosa morphology ( J:178053 )

• DSS-treated mice exhibit thickened submucosa compared with similarly treated wild-type mice

abnormal intestinal goblet cell morphology ( J:178053 )

• decreased in DSS-treated mice compared with similarly treated wild-type mice

abnormal crypts of Lieberkuhn morphology ( J:178053 )

• DSS-treated mice exhibit loss of morphology and crypt architecture compared with similarly treated wild-type mice

intestinal ulcer ( J:178053 )

• in DSS-treated mice

abnormal gut flora balance ( J:178053 )

• reduced segmented filamentous bacteria group

increased susceptibility to induced colitis ( J:178053 )

• DDS-treated mice exhibit extremely severe intestinal bleeding with moderate hyperplasia of the lamina propria, thickened submucosa, loss of morphology and crypt architecture, progressive complete loss of colonic epithelial layer, decrease in goblet cells, and severe ulceration; accelerated and increased weight loss; and accelerated and higher mortality compared with similarly treated wild-type mice

• intermediate phenotype to Pglyrp2^tm1Rdz or Pglyrp3^tm1Rdz and Pglyrp4^tm1Rdz homozygotes

• mice exhibit increased sensitivity to DSS-induced colitis at 3% or 5% DSS compared with wild-type mice

immune system

increased susceptibility to induced colitis ( J:178053 )

• DDS-treated mice exhibit extremely severe intestinal bleeding with moderate hyperplasia of the lamina propria, thickened submucosa, loss of morphology and crypt architecture, progressive complete loss of colonic epithelial layer, decrease in goblet cells, and severe ulceration; accelerated and increased weight loss; and accelerated and higher mortality compared with similarly treated wild-type mice

• intermediate phenotype to Pglyrp2^tm1Rdz or Pglyrp3^tm1Rdz and Pglyrp4^tm1Rdz homozygotes

• mice exhibit increased sensitivity to DSS-induced colitis at 3% or 5% DSS compared with wild-type mice

abnormal chemokine secretion ( J:178053 )

• induced mouse embryonic fibroblasts and peritoneal macrophage exhibit increased CXCL1 production compared with wild-type cells

increased interleukin-6 secretion ( J:178053 )

• in induced mouse embryonic fibroblasts and peritoneal macrophage

cardiovascular system

gastrointestinal hemorrhage ( J:178053 )

• severe in DSS-treated mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:178053 )

• DSS-treated mice exhibit loss of morphology and crypt architecture compared with similarly treated wild-type mice

growth/size/body

weight loss ( J:178053 )

• severe in DSS-treated mice

homeostasis/metabolism

increased susceptibility to xenobiotic induced morbidity/mortality ( J:178053 )

• in DSS-treated mice

cellular

abnormal intestinal goblet cell morphology ( J:178053 )

• decreased in DSS-treated mice compared with similarly treated wild-type mice

Genotype
MGI:5297115

cx4

• Allelic Composition: Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz; Pglyrp2^tm1Rdz/Pglyrp2^tm1Rdz
• Genetic Background: C.129S-Pglyrp1^tm1Rdz Pglyrp2^tm1Rdz

immune system

decreased susceptibility to induced arthritis ( J:178054 )

• in response to peptidoglycan or muramyl dipeptide (MDP), mice develop less severity and incidence in arthritis compared similarly treated wild-type mice but not to the same extent as in Pglyrp2^tm1Rdz homozygotes

skeleton

decreased susceptibility to induced arthritis ( J:178054 )

• in response to peptidoglycan or muramyl dipeptide (MDP), mice develop less severity and incidence in arthritis compared similarly treated wild-type mice but not to the same extent as in Pglyrp2^tm1Rdz homozygotes