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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Anxa7tm1Pll
targeted mutation 1, Harvey B Pollard
MGI:2159005
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Anxa7tm1Pll/Anxa7tm1Pll Not Specified MGI:3588100
ht2
Anxa7tm1Pll/Anxa7+ B6.Cg-Anxa7tm1Pll MGI:3588102
ht3
Anxa7tm1Pll/Anxa7+ Not Specified MGI:3588101


Genotype
MGI:3588100
hm1
Allelic
Composition
Anxa7tm1Pll/Anxa7tm1Pll
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Anxa7tm1Pll mutation (0 available); any Anxa7 mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygous mutant embryos die at ~E10 due to cardiovascular defects; no viable embryos are obtained at E11

cardiovascular system
• at E10, 8 of 40 mutant embryos display hemorrhages into the brain vesicles in the absence of other developmental anomalies
• such hemorrhages are composed of both mature maternal erythrocytes and fetal nucleated erythroid precursors

nervous system
• at E10, 8 of 40 mutant embryos display hemorrhages into the brain vesicles in the absence of other developmental anomalies
• such hemorrhages are composed of both mature maternal erythrocytes and fetal nucleated erythroid precursors




Genotype
MGI:3588102
ht2
Allelic
Composition
Anxa7tm1Pll/Anxa7+
Genetic
Background
B6.Cg-Anxa7tm1Pll
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Anxa7tm1Pll mutation (0 available); any Anxa7 mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Metastatic lymphosarcoma of the thymus in Anxa7tm1Pll/Anxa7+ mice

neoplasm
• although tumors occur in both heterozygous males and females, females exhibit a higher propensity for tumor development
• by ~1 year of age, ~23% of heterozygotes have developed visible spontaneous tumors (~1-cm or greater in diameter)
• 42% of heterozygotes with visible tumors exhibit lesions in multiple locations
• among 58 males and 79 females analyzed, 1 primary colon tumor was detected in a male, and 2 primary lung tumors were detected in females; single instances of prostate carcinoma, ovarian carcinoma, and salivary gland tumors were observed
• both male and female heterozygotes develop hepatocellular carcinomas
• lymphoid tumors involving thymus and spleen comprise 50% and 76% of visible tumors detected in heterozygous males and females, respectively
• frequent diagnoses include lymphosarcomas of the thymus, both localized and metastatic to the lung or pancreas

liver/biliary system
• both male and female heterozygotes develop hepatocellular carcinomas

growth/size/body
• heterozygous males display gigantism in the absence of obesity
• in males, increased growth rate continues uninterrupted for at least one year, leading to 40- to 60-g mice (~25% increase in body weight relative to wild-type)
• in addition, a number of internal organs increase in weight proportionately
• after postnatal week 4, heterozygous males show a significantly enhanced growth spurt relative to wild-type males
• in contrast, heterozygous females show normal growth curves as a function of age

cellular
• spectral karyotyping indicates that hepatocellular carcinomas display chromosomal instability and clonal chromosomal aberrations, with genomic changes on chromosomes 3, 4, 5, 8, 9, 12, 14, and 19
• moreover, gene-expression profiling of tumors indicates down-regulation of several specific tumor suppressor and DNA-repair genes, contributing to the cancer-prone phenotype

endocrine/exocrine glands
N
• the pituitaries of heterozygous males and females appear histologically normal
• heterozygous males exhibit normal plasma insulin-like growth factor 1 and corticosterone levels
• in addition, no changes in luteinizing hormone, growth hormone, thyrotropin, prolactin, alpha-melanocyte-stimulating hormone, beta-endorphin, or corticotropin levels are observed




Genotype
MGI:3588101
ht3
Allelic
Composition
Anxa7tm1Pll/Anxa7+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Anxa7tm1Pll mutation (0 available); any Anxa7 mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Islet hyperplasia in Anxa7tm1Pll/Anxa7+ mice

endocrine/exocrine glands
• at ~3 months, both female and male heterozygotes show beta cell hypertrophy
• the average diameters of heterozygous beta cells are ~75% greater than those of wild-type beta cells
• at ~3 months, heterozygotes display significantly enlarged islets relative to wild-type
• starting at ~6 weeks, both female and male heterozygotes display islet cell hyperplasia
• the insulin-containing secretory vesicles in mutant beta cells display an ~2-fold increase in insulin relative to vesicles in wild-type beta cells
• heterozygous mutants show no significant differences in insulin tolerance tests relative to wild-type mice
• isolated heterozygous islets show a significant defect in calcium-dependent insulin secretion, despite an observed 8- to 10-fold increase in the levels of total insulin; impaired insulin secretion is probably caused by altered Ca2+ signaling
• glucose metabolism, KATP channels, and voltage-gated channels remain functionally intact in mutant beta cells
• at ~3 months, heterozygotes exhibit a mild inflammatory invasion of the pancreatic duct

homeostasis/metabolism
• heterozygous mutants show no significant differences in insulin tolerance tests relative to wild-type mice
• isolated heterozygous islets show a significant defect in calcium-dependent insulin secretion, despite an observed 8- to 10-fold increase in the levels of total insulin; impaired insulin secretion is probably caused by altered Ca2+ signaling
• glucose metabolism, KATP channels, and voltage-gated channels remain functionally intact in mutant beta cells
• heterozygotes exhibit Ca2+-dependent endocrine secretory defects, suggesting that annexin A7 is involved in Ca2+ signaling and/or Ca2+ homeostasis
• heterozygotes show altered expression of the inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] receptor and a resulting failure of Ins(1,4,5)P3-induced Ca2+ release from internal stores, which is typically required for insulin secretion from pancreatic islet cells

immune system
• at ~3 months, heterozygotes exhibit a mild inflammatory invasion of the pancreatic duct





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last database update
11/14/2017
MGI 6.11
The Jackson Laboratory