All Phenotypes Sult1e1<tm1Song> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Sult1e1^tm1Song/Sult1e1^tm1Song	B6.129S6-Sult1e1^tm1Song	MGI:3529677
hm2	Sult1e1^tm1Song/Sult1e1^tm1Song	involves: 129S6/SvEvTac * C57BL/6	MGI:3529670

Allelic Composition	Sult1e1^tm1Song/Sult1e1^tm1Song
Genetic Background	B6.129S6-Sult1e1^tm1Song

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sult1e1^tm1Song mutation (0 available); any Sult1e1 mutation (20 available)

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

hematopoietic system

abnormal platelet physiology ( J:96050 )

• pregnant homozygous null females showed increased platelet sensitivity to agonist-induced activation than wild-type

homeostasis/metabolism

abnormal platelet physiology ( J:96050 )

• pregnant homozygous null females showed increased platelet sensitivity to agonist-induced activation than wild-type

increased circulating estradiol level ( J:96050 )

• serum estradiol levels in pregnant homozygous null females from 12.5 dpc to 17.5 dpc were significantly elevated

abnormal placental thrombosis ( J:96050 )

• homozygous null females exhibited placental thrombosis and degeneration as evidenced by darker and enlarged placentas, hemorrhages and extensive tissue necrosis that was independent of embryo genotype

abnormal amniotic fluid composition ( J:96050 )

• homozygous null females showed an increase in the free estradiol levels in the amniotic fluids of fetuses at 14.5, 16.5, and 17.5 dpc

reproductive system

reduced female fertility ( J:96050 )

• homozygous null females produced fewer and smaller litters (when mated to either null or wild-type males) and had significantly fewer healthy fetuses than wild-type between 12.5 dpc and 17.5 dpc (but not at 11.5 dpc), and this reduction was accompanied by the presence of dead or reabsorbed fetuses, indicating spontaneous fetal loss

• treatment of pregnant homozygous null mice with either an anticoagulant or antiestrogen prevented fetal loss

decreased litter size ( J:96050 )

• litter sizes in crosses between homozygous null mice were on average 50% smaller than wild-type

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

endocrine/exocrine glands

increased seminal vesicle weight ( J:96133 )

• the seminal vesicle/coagulating gland had a significantly increased wet weight because of tissue swelling

abnormal testis morphology ( J:96133 )

• presence of numerous giant yellow cells that contained multiple dark stained nuclei in the hyperplastic lesions found in the peripheral space as well as in Leydig cell clusters located at inner tubular junctions of the testis

• observed a thickening of the capsule of the testis

abnormal seminiferous tubule morphology ( J:96133 )

• seminiferous tubules were filled with vacuoles and had disrupted spermatogenic epithelium in 12 month or older mutant mice

abnormal Leydig cell morphology ( J:96133 )

• cytoplasm of Leydig cells contained vacuoles and stained less uniformly with eosin than controls

Leydig cell hypertrophy ( J:96133 )

• Leydig cell hypertrophy was commonly observed within inner tubular junctions

• presence of masses of hypertrophic Leydig cells with volumes 2-3 times larger than normal in 12 month or older mutant testes but not in 2 month old mice

increased Leydig cell number ( J:96133 )

• hyperplasia occurred more frequently in the peripheral space under the testicular capsule

decreased testis weight ( J:96133 )

• significant reduction in the relative weight of the testis of 18- to 22- month old but not 3-month old mutants

reproductive system

abnormal sperm motility ( J:96133 )

• total and forward motility of caudal sperm was reduced by 60% in 18-month old mutants and 80% in 22-month old mutants but not in 3-month old males