Overview

Also Known As:opossum

These mice carry a spontaneous mutation at the Sox18 locus characterized by a delayed coat development, failure of skin darkening, and paucity of fur.

Genetic overview

Genetic Background	Generation

Sox18^Ra-Op

Allele Type	Gene Symbol	Gene Name
Spontaneous	Sox18	SRY (sex determining region Y)-box 18

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Research Applications

Dermatology Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The Sox18^Ra-Op allele causes a more severe phenotype than either the Sox18^Ra or Sox18^Ra-J allele. Green and Mann determined that only approximately 17% of the Sox18^Ra-Op/+ heterozygotes are born and survive to wean age. Heterozygotes have a deficiency of vibrissae, a distinguishing feature in utero and usually evident at birth, and can be distinguished at three days of age by their pink skin which, with its delayed coat development, fails to darken like that of wildtype siblings. A paucity of fur is apparent by 9 days of age and persists throughout life. Heterozygotes are smaller in overall size and many of those that die shortly after birth are cyanotic and edematous. Dead pups have glossy skin with red patches that may result from superficial hemorrhages. Homozygotes die by embryonic day 11.5. (Green and Mann, 1961; Mann, 1963.)

Genetics

Sox18^Ra-Op

Allele Symbol: Sox18^Ra-Op

Allele Name	opossum
Allele Type	Spontaneous
Allele Synonym(s)	Op; Ra^Op
Gene Symbol and Name	Sox18, SRY (sex determining region Y)-box 18
Gene Synonym(s)
Strain of Origin	(C57BL/6J x DBA/2J)F1
Chromosome	2
Molecular Note	The mutation was identified as a deletion of a single cytosine at nucleotide 1048.

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Sox18^Ra-Op related

Dermatology Research
- Skin and Hair Texture Defects

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: Sox18^Ra-Op/Sox18^Ra-Op
B6D2-Sox18/J

homeostasis/metabolism phenotype

edema
- generalized at E13.5

skin edema
- 63% of mice exhibit severe subcutaneous edema in the trunk and neck regions un like in wild-type mice
- at E13.5

immune system phenotype

abnormal lymphatic vessel morphology
- lymphatic vessels are finer, denser, and more branched with more loops and fewer blind-ended sacs compared to in wild-type mice

integument phenotype

skin edema
- at E13.5
- 63% of mice exhibit severe subcutaneous edema in the trunk and neck regions un like in wild-type mice

mammalian phenotype

cardiovascular system phenotype
- Normal - between E8.5 and E10.5, differentiation, proliferation, migration and association of endothelial cells, and patterning and establishment of the primary vascular plexus is normal

mortality/aging

lethality throughout fetal growth and development, complete penetrance
- mice die before E14.5
- mice do not survive beyond E14.5

cardiovascular system phenotype

abnormal blood vessel morphology
- at E14.5, surface microvessels, particularly around the anterior cranial region, are enlarged compared to in wild-type mice
- enlarged blood vessels frequently rupture
- at E13.5, all mice exhibit enlarged surface microvasculature compared to in wild-type mice
- vascular defects increase in severity with age
- at E12.5, 67% of mice exhibit enlarged surface microvasculature in the trunk, head, proximal limb and neck unlike in wild-type mice
- subdermal microvasculature diameter is increased 21% at E12.5 and 35% at E13.5 compared to in wild-type mice

hemorrhage
- at E14.5, large-scale vascular hemorrhage is observed in all mice
- enlarged blood vessels frequently rupture
- at E13.5, mice exhibit multiple regions of vascular hemorrhage unlike in wild-type mice

abnormal pericyte morphology
- fewer pericytes are recruited to microvasculature compared to in wild-type mice

hematoma
- over large areas of the trunk, neck, and head

increased vascular endothelial cell number
- endothelial hyperplasia is associated with defects in pericyte recruitment

abnormal vascular endothelial cell physiology
- loss of vascular integrity is due to endothelial rupture

Genotype: Sox18^Ra-Op/Sox18⁺
involves: C57BL/6J * DBA/2J

integument phenotype

abnormal vibrissa morphology
- postoral and posterior supra-orbital vibrassa are decreased in number compared to in wild-type mice
- at E17, mystacial vibrissa are incomplete and post-orbital vibrissa are absent or reduced in size compared to in wild-type mice
- mice lack inter-ramal and anterior supra-orbital vibrissa unlike wild-type mice

decreased zigzag hair amount
- zigzag hairs are absent in the middle of the dorsum
- only a small patch on the shoulders

delayed hair appearance
- at 3 days of age, mice are still pink due to sparse coat unlike wild-type mice that have developed a coat
- initiation of each follicle type is delayed compared to in wild-type mice

abnormal hair follicle morphology
- mice lack follicles in the quiescent stage and are abnormal with bulbs that are twisted and curved unlike in wild-type mice

abnormal hair growth
- asynchronous

abnormal zigzag hair morphology
- some zigzag hairs are narrow, curled, lacked constrictions, and contain small medullar cells which lack pigment unlike in wild-type mice

short vibrissae
- at E17, post-orbital vibrissa are shorter than normal

abnormal awl hair morphology
- mice have some awl hairs unlike in wild-type mice

abnormal vibrissa number
- anterior vibrissae and their follicles are absent unlike in wild-type mice

skin edema
- mice that die around birth have edematous skin that is stretched, glossy, membranous in appearance, with red patches

absent auchene hairs

sparse hair

growth/size/body region phenotype

decreased body size
- at weaning mice are two-thirds the size of wild-type mice
- mice are smaller than normal from birth up to three months of age

distended abdomen
- mice that die prior to weaning exhibit swollen abdomens with perintoneal cavities filled with thin, white liquid unlike in wild-type mice

mortality/aging

perinatal lethality, incomplete penetrance
- many mice are dead or dying shortly after birth
- many mice are dead or dying at birth

postnatal lethality, incomplete penetrance
- edematous mice die prior to weaning
- fewer than expected mice are present at weaning

homeostasis/metabolism phenotype

skin edema
- mice that die around birth have edematous skin that is stretched, glossy, membranous in appearance, with red patches

edema
- at birth, some mice are edematous
- mice that die around birth are edematous in the neck, shoulders, and abdominal and pleural cavities

cyanosis
- in some mice at birth

Genotype: Sox18^Ra-Op/Sox18^Ra-Op
involves: C57BL/6J * DBA/2J

mortality/aging

embryonic lethality, complete penetrance
- mice die at E11 or earlier

preweaning lethality, complete penetrance
- no mice are found (no time of observation provided)

References

Additional References

Dunn TL; Mynett-Johnson L; Wright EM; Hosking BM; Koopman PA; Muscat GE. 1995. Sequence and expression of Sox-18 encoding a new HMG-box transcription factor. Gene 161(2):223-5PubMed: 7665083 MGI: J:28369
Hosking BM; Wyeth JR; Pennisi DJ; Wang SC; Koopman P; Muscat GE. 2001. Cloning and functional analysis of the Sry-related HMG box gene, Sox18. Gene 262(1-2):239-47PubMed: 11179689 MGI: J:67559
James K; Hosking B; Gardner J; Muscat GE; Koopman P. 2003. Sox18 mutations in the ragged mouse alleles ragged-like and opossum. Genesis 36(1):1-6PubMed: 12748961 MGI: J:83731
Pennisi D; Bowles J; Nagy A; Muscat G; Koopman P. 2000. Mice null for sox18 are viable and display a mild coat defect Mol Cell Biol 20(24):9331-6PubMed: 11094083 MGI: J:66010
Pennisi D; Gardner J; Chambers D; Hosking B; Peters J; Muscat G; Abbott C; Koopman P. 2000. Mutations in Sox18 underlie cardiovascular and hair follicle defects in ragged mice. Nat Genet 24(4):434-7PubMed: 10742113 MGI: J:61488

Additional - Sox18^Ra-Op related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Genotyping resources and troubleshooting
Breeding Considerations

Homozygotes are embryonic lethal. Heterozygous females are poor breeders, and some heterozygotes may die at birth. When maintaining a live colony, wildtype females from the colony may be bred to heterozygous males.
- Additional Breeding and Husbandry Support
Citation
When using the opossum mouse strain in a publication, please cite the originating article(s) and include JAX stock #000508 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

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Live Mouse

Age

Genotype

Price

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Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous for Ra-Op>

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:opossum

Genetic overview

Research Applications

Base Price

Detailed Description

Sox18Ra-Op

Allele Symbol: Sox18Ra-Op

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Sox18Ra-Op related

Mammalian Phenotype Terms by Genotype

Genotype: Sox18Ra-Op/Sox18Ra-OpB6D2-Sox18/J

homeostasis/metabolism phenotype

immune system phenotype

integument phenotype

mammalian phenotype

mortality/aging

cardiovascular system phenotype

Genotype: Sox18Ra-Op/Sox18+involves: C57BL/6J * DBA/2J

integument phenotype

growth/size/body region phenotype

mortality/aging

homeostasis/metabolism phenotype

Genotype: Sox18Ra-Op/Sox18Ra-Opinvolves: C57BL/6J * DBA/2J

mortality/aging

References

Additional References

Additional - Sox18Ra-Op related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Sox18^Ra-Op

Allele Symbol: Sox18^Ra-Op

Genotype: Sox18^Ra-Op related

Genotype: Sox18^Ra-Op/Sox18^Ra-Op
B6D2-Sox18/J

Genotype: Sox18^Ra-Op/Sox18⁺
involves: C57BL/6J * DBA/2J

Genotype: Sox18^Ra-Op/Sox18^Ra-Op
involves: C57BL/6J * DBA/2J

Additional - Sox18^Ra-Op related