Phenotypes associated with this allele

• Allele Symbol: Tigar^tm1.2Smat
• Allele Name: targeted mutation 1.2, Satoaki Matoba
• Allele ID: MGI:5319187
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Tigar^tm1.2Smat/Tigar^tm1.2Smat Tg(CAG-EGFP/Map1lc3b)53Nmz/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6JJcl * C57BL/6NCrj	MGI:5319196

Genotype
MGI:5319196

cx1

• Allelic Composition: Tigar^tm1.2Smat/Tigar^tm1.2Smat; Tg(CAG-EGFP/Map1lc3b)53Nmz/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6JJcl * C57BL/6NCrj

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

cardiovascular system

abnormal heart morphology ( J:183674 )

• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice

increased cardiac muscle contractility ( J:183674 )

• following myocardial infarction

abnormal response to cardiac infarction ( J:183674 )

• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice

• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice

cellular

abnormal mitochondrial chromosome morphology ( J:183674 )

• following myocardial infarction, cardiac muscles exhibit decreased mitochondria DNA damage compared to in wild-type mice

• however, treatment with chloroquine elevates mitochondria DNA damage to wild-type levels

abnormal autophagy ( J:183674 )

• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice

decreased cardiomyocyte apoptosis ( J:183674 )

• following myocardial infarction

abnormal mitochondrial physiology ( J:183674 )

• following myocardial infarction, cardiac muscles exhibit increased mitophagy compared to in wild-type mice

• however, treatment with chloroquine elevates mitochondrial to wild-type levels

oxidative stress ( J:183674 )

• following myocardial infarction, cardiac muscles exhibit increased levels of reactive oxygen species production compared to in wild-type mice

homeostasis/metabolism

abnormal response to cardiac infarction ( J:183674 )

• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice

• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice

abnormal autophagy ( J:183674 )

• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice

muscle

increased cardiac muscle contractility ( J:183674 )

• following myocardial infarction

decreased cardiomyocyte apoptosis ( J:183674 )

• following myocardial infarction