Phenotypes associated with this allele

• Allele Symbol: Pglyrp2^tm1Rdz
• Allele Name: targeted mutation 1, Roman Dziarski
• Allele ID: MGI:5297105
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Pglyrp2^tm1Rdz/Pglyrp2^tm1Rdz	C.129S-Pglyrp2^tm1Rdz	MGI:5297112
hm2	Pglyrp2^tm1Rdz/Pglyrp2^tm1Rdz	involves: 129S/SvEv * BALB/c	MGI:5297161
cx3	Pglyrp1^tm1Rdz/Pglyrp1^tm1Rdz Pglyrp2^tm1Rdz/Pglyrp2^tm1Rdz	C.129S-Pglyrp1^tm1Rdz Pglyrp2^tm1Rdz	MGI:5297115

Genotype
MGI:5297112

hm1

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

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

immune system

abnormal circulating chemokine level ( J:178054 )

• mice treated with peptidoglycan and muramyl dipeptide (MDP) exhibit lower chemokine (CCL2, CCL12, and CXCL1) that in similarly treated wild-type mice

decreased susceptibility to induced arthritis ( J:178054 )

• in response to peptidoglycan or muramyl dipeptide (MDP), mice fail to develop acute tendonitis or arthritis unlike similarly treated wild-type mice

skeleton

decreased susceptibility to induced arthritis ( J:178054 )

• in response to peptidoglycan or muramyl dipeptide (MDP), mice fail to develop acute tendonitis or arthritis unlike similarly treated wild-type mice

homeostasis/metabolism

abnormal circulating chemokine level ( J:178054 )

• mice treated with peptidoglycan and muramyl dipeptide (MDP) exhibit lower chemokine (CCL2, CCL12, and CXCL1) that in similarly treated wild-type mice

Genotype
MGI:5297161

hm2

• Allelic Composition: Pglyrp2^tm1Rdz/Pglyrp2^tm1Rdz
• Genetic Background: involves: 129S/SvEv * 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 extensive 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 Lactobacillus/Lactococcus, segmented filamentous bacteria, Clostridium perfringens, and Bacteroides groups

increased susceptibility to induced colitis ( J:178053 )

• DDS-treated mice exhibit extremely severe intestinal bleeding with extensive 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

• more severe than in Pglyrp1^tm1Rdz and Pglyrp4^tm1Rdz homozygotes

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

• stool induces increased sensitivity to DSS-induced colitis compared with stool from wild-type mice

immune system

increased susceptibility to induced colitis ( J:178053 )

• DDS-treated mice exhibit extremely severe intestinal bleeding with extensive 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

• more severe than in Pglyrp1^tm1Rdz and Pglyrp4^tm1Rdz homozygotes

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

• stool induces increased sensitivity to DSS-induced colitis compared with stool from 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

cx3

• 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