All Phenotypes Elavl1<tm1.1Dkon> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Elavl1^tm1.1Dkon/Elavl1^tm1.1Dkon Lyz2^tm1(cre)Ifo/Lyz2⁺	B6.129P2-Elavl1^tm1.1Dkon Lyz2^tm1(cre)Ifo	MGI:5429343
cn2	Elavl1^tm1.1Dkon/Elavl1^tm1.1Dkon Tg(MYOD1-cre)M23Glh/0	involves: 129P2/OlaHsd * C57BL/6	MGI:6363424
cn3	Elavl1^tm1.1Dkon/Elavl1^tm1.1Dkon Lyz2^tm1(cre)Ifo/Lyz2⁺	involves: 129P2/OlaHsd * C57BL/6J	MGI:5429344

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

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:184388 )

• in response to LPS treatment, mice exhibit increased lethality compared with control mice

immune system

immune system phenotype ( J:184388 )

N	• mice exhibit normal myelopoiesis

abnormal macrophage chemotaxis ( J:184388 )

• enhanced in response to CCR2 signals

increased susceptibility to induced colitis ( J:184388 )

• DSS-treated mice exhibit enhanced progression and maintenance of inflammatory colitis and 2 of 19 mice develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice

increased macrophage cell number ( J:184388 )

increased monocyte cell number ( J:184388 )

increased circulating interleukin-1 beta level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-12 level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-6 level ( J:184388 )

• in response to LPS treatment

increased circulating tumor necrosis factor level ( J:184388 )

• in response to LPS treatment

increased susceptibility to endotoxin shock ( J:184388 )

• in response to LPS treatment, mice exhibit increased lethality and increased serum levels of TNF, IL6, IL1B and IL12 compared with control mice

neoplasm

increased colon adenoma incidence ( J:184388 )

• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice

increased colon adenocarcinoma incidence ( J:184388 )

• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice

increased incidence of tumors by chemical induction ( J:184388 )

• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice

• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice

increased tumor growth/size ( J:184388 )

• in mice treated with DSS and DMH

digestive/alimentary system

increased colon adenoma incidence ( J:184388 )

• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice

increased colon adenocarcinoma incidence ( J:184388 )

• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice

increased susceptibility to induced colitis ( J:184388 )

homeostasis/metabolism

increased circulating interleukin-1 beta level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-12 level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-6 level ( J:184388 )

• in response to LPS treatment

increased circulating tumor necrosis factor level ( J:184388 )

• in response to LPS treatment

increased susceptibility to xenobiotic induced morbidity/mortality ( J:184388 )

• in response to LPS treatment, mice exhibit increased lethality compared with control mice

increased incidence of tumors by chemical induction ( J:184388 )

• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice

• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice

cellular

abnormal macrophage chemotaxis ( J:184388 )

• enhanced in response to CCR2 signals

hematopoietic system

abnormal macrophage chemotaxis ( J:184388 )

• enhanced in response to CCR2 signals

increased macrophage cell number ( J:184388 )

increased monocyte cell number ( J:184388 )

Allelic Composition	Elavl1^tm1.1Dkon/Elavl1^tm1.1Dkon Tg(MYOD1-cre)M23Glh/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Elavl1^tm1.1Dkon mutation (0 available); any Elavl1 mutation (43 available)
Tg(MYOD1-cre)M23Glh mutation (0 available)

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

homeostasis/metabolism

increased carbon dioxide production ( J:279284 )

• mice show a higher rate of carbon dioxide production than control littermates

increased oxygen consumption ( J:279284 )

• mice show a higher rate of oxygen consumption than control littermates

increased respiratory quotient ( J:279284 )

• mice show a slight increase in the respiratory exchange ratio (RER), that is most evident during the peak of voluntary movement

• however, heat production levels and ambulatory activity are normal

enhanced exercise endurance ( J:279284 )

• in a treadmill exhaustion test, mice perform 20% more work than control mice; the time to exhaustion and the running distance covered is significantly longer than that in control mice

• in an accelerating Rota-rod system, the latency to fall is significantly increased relative to that in control mice

increased aerobic running capacity ( J:279284 )

• in a treadmill exhaustion test, the running distance covered is significantly longer than that in control mice

muscle

abnormal skeletal muscle fiber type ratio ( J:279284 )

• soleus muscle shows a ~17% enrichment of oxidative type I fibers, while type IIA fibers are decreased by ~16% relative to those in control mice; similar effects on the proportion of type I fibers are observed in the peroneus and EDL muscles

• however, mean cross sectional area of soleus muscle fibers is normal

decreased susceptibility to induced muscular atrophy ( J:279284 )

• in the Lewis Lung Carcinoma (LLC)-induced muscle wasting model, mice show a significant protection from LLC-induced weight loss with significantly lower atrophy in several hindlimb muscles, including gastrocnemius, TA, soleus and peroneus, and increased cross sectional area of muscle fibers relative to LLC-control mice

• however, no differences in tumor growth, tumor burden or levels of systemic inflammatory response are observed

abnormal muscle contractility ( J:279284 )

• in situ analysis of muscle contractility revealed that tibialis anterior (TA) muscles generate a higher contraction force than those of control mice

• however, no differences are observed in the fatigability test

cellular

abnormal mitochondrial ATP synthesis coupled electron transport ( J:279284 )

• several key components of the electron transport chain complexes including CIII and CIV, as well as the ATP synthase CV, are upregulated in muscles

Allelic Composition	Elavl1^tm1.1Dkon/Elavl1^tm1.1Dkon Lyz2^tm1(cre)Ifo/Lyz2⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Elavl1^tm1.1Dkon mutation (0 available); any Elavl1 mutation (43 available)
Lyz2^tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (41 available)

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

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:184388 )

• in response to LPS treatment, mice exhibit increased lethality compared with control mice

immune system

immune system phenotype ( J:184388 )

N	• mice exhibit normal myelopoiesis

increased circulating interleukin-1 beta level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-12 level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-6 level ( J:184388 )

• in response to LPS treatment

increased circulating tumor necrosis factor level ( J:184388 )

• in response to LPS treatment

increased susceptibility to endotoxin shock ( J:184388 )

• in response to LPS treatment, mice exhibit increased lethality and increased serum levels of TNF, IL6, IL1B and IL12 compared with control mice

homeostasis/metabolism

increased circulating interleukin-1 beta level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-12 level ( J:184388 )

• in response to LPS treatment

increased circulating interleukin-6 level ( J:184388 )

• in response to LPS treatment

increased circulating tumor necrosis factor level ( J:184388 )

• in response to LPS treatment

increased susceptibility to xenobiotic induced morbidity/mortality ( J:184388 )

• in response to LPS treatment, mice exhibit increased lethality compared with control mice

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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