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 (42 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 (42 available)
Lyz2^tm1(cre)Ifo mutation (16 available); any Lyz2 mutation (40 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)
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support.	last database update 09/30/2025 MGI 6.24