Phenotypes associated with this allele

• Allele Symbol: Lncucc1^em1Bwu
• Allele Name: endonuclease-mediated mutation 1, Baojian Wu
• Allele ID: MGI:7571572
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Lncucc1^em1Bwu/Lncucc1^em1Bwu	C57BL/6-Lncucc1^em1Bwu	MGI:7614804

Genotype
MGI:7614804

hm1

• Allelic Composition: Lncucc1^em1Bwu/Lncucc1^em1Bwu
• Genetic Background: C57BL/6-Lncucc1^em1Bwu

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

digestive/alimentary system

decreased colon length ( J:340220 )

• DSS-treated mice exhibit a significantly shorter colon length than DSS-treated wild-type controls

abnormal intestine physiology ( J:340220 )

• mRNA and protein expression of the circadian clock gene Nr1d1 (aka Rev-erbalpha, a dual NF-kappaB/Nlrp3 repressor) is markedly downregulated in the colon and its diurnal rhythm is blunted

increased enterocyte apoptosis ( J:340220 )

• DSS-treated mice exhibit aggravated cell apoptosis in the colon, as indicated by immunohistochemistry for cleaved caspase-3

abnormal enterocyte proliferation ( J:340220 )

• DSS-treated mice exhibit reduced cell proliferation in the colon, as indicated by immunofluorescence for Ki67

abnormal susceptibility to colitis induced morbidity/mortality ( J:340220 )

• after treatment with oxazolone to induce colitis at different circadian points, mice show loss of diurnal rhythmicity in colitis severity with no significant difference in survival time (h) between Z10 and Z22, unlike in oxazolone-treated wild-type controls which display a marked diurnal rhythm in survival time (most severe at ZT22 and least severe at ZT6)

increased susceptibility to induced colitis ( J:340220 )

• mice show increased sensitivity to dextran sulfate sodium (DSS)-induced colitis with more extensive weight loss, higher disease activity index (DAI), shorter colons, greater myeloperoxidase (MPO) activity, histopathological scores and infiltration of F4/80+ macrophages, increased cell apoptosis, and lower cell proliferation than DSS-treated wild-type controls

• moreover, colonic protein levels of phosphorylated p65 and mature caspase-1 as well as colonic expression of proinflammatory cytokines (IL-1beta and IL-6) are higher than in DSS-treated wild-type controls, indicating exacerbated activation of NF-kappaB signaling and Nlrp3 inflammasome

• during DSS treatment, mice show a more extensive reduction in colonic Nr1d1 (Rev-erbalpha) expression than wild-type controls

immune system

abnormal susceptibility to colitis induced morbidity/mortality ( J:340220 )

• after treatment with oxazolone to induce colitis at different circadian points, mice show loss of diurnal rhythmicity in colitis severity with no significant difference in survival time (h) between Z10 and Z22, unlike in oxazolone-treated wild-type controls which display a marked diurnal rhythm in survival time (most severe at ZT22 and least severe at ZT6)

increased susceptibility to induced colitis ( J:340220 )

• mice show increased sensitivity to dextran sulfate sodium (DSS)-induced colitis with more extensive weight loss, higher disease activity index (DAI), shorter colons, greater myeloperoxidase (MPO) activity, histopathological scores and infiltration of F4/80+ macrophages, increased cell apoptosis, and lower cell proliferation than DSS-treated wild-type controls

• moreover, colonic protein levels of phosphorylated p65 and mature caspase-1 as well as colonic expression of proinflammatory cytokines (IL-1beta and IL-6) are higher than in DSS-treated wild-type controls, indicating exacerbated activation of NF-kappaB signaling and Nlrp3 inflammasome

• during DSS treatment, mice show a more extensive reduction in colonic Nr1d1 (Rev-erbalpha) expression than wild-type controls

cellular

increased enterocyte apoptosis ( J:340220 )

• DSS-treated mice exhibit aggravated cell apoptosis in the colon, as indicated by immunohistochemistry for cleaved caspase-3

abnormal enterocyte proliferation ( J:340220 )

• DSS-treated mice exhibit reduced cell proliferation in the colon, as indicated by immunofluorescence for Ki67

mortality/aging

abnormal susceptibility to colitis induced morbidity/mortality ( J:340220 )

• after treatment with oxazolone to induce colitis at different circadian points, mice show loss of diurnal rhythmicity in colitis severity with no significant difference in survival time (h) between Z10 and Z22, unlike in oxazolone-treated wild-type controls which display a marked diurnal rhythm in survival time (most severe at ZT22 and least severe at ZT6)