Figure 3
Figure 3. Deletion of Mfrn1 in adult mice leads to loss of Mfrn1 in hematopoietic tissues. Mfrn1flox/− mice were crossed to mice carrying Mx-Cre. At 3 weeks of age, mice (Mfrn1flox/−;Mx-Cre) were injected with poly(I:C) to induce Cre expression. The mice were analyzed 4-8 weeks later. (A) PCR analysis of Mfrn1 of genomic DNA from thymus (T), spleen (S), liver (L), and bone marrow (Bm) of mice with noted genotypes. (B) RT-PCR analysis of mRNA in the spleens of mice with the noted genotypes using primers specific to exon1 and exon4, which flank exon 2. A wild-type mRNA gave rise to a transcript amplification of 443 bp; a deletion of exon 2 at genomic level gave rise to a transcript amplification of 214 bp. (C) Western analysis of Mfrn1, porin, and tubulin in cytosol, mitochondria, and total bone marrow isolated from mice with the specified genotypes. (D) Bar graph of spleen weight/total weight of mice with the noted genotypes. (E). Hematoxylin and eosin–stained sections of spleen from Mfrn1+/+ mice and Mx-Cre–deleted Mfrn1−/− mice.

Deletion of Mfrn1 in adult mice leads to loss of Mfrn1 in hematopoietic tissues.Mfrn1flox/− mice were crossed to mice carrying Mx-Cre. At 3 weeks of age, mice (Mfrn1flox/−;Mx-Cre) were injected with poly(I:C) to induce Cre expression. The mice were analyzed 4-8 weeks later. (A) PCR analysis of Mfrn1 of genomic DNA from thymus (T), spleen (S), liver (L), and bone marrow (Bm) of mice with noted genotypes. (B) RT-PCR analysis of mRNA in the spleens of mice with the noted genotypes using primers specific to exon1 and exon4, which flank exon 2. A wild-type mRNA gave rise to a transcript amplification of 443 bp; a deletion of exon 2 at genomic level gave rise to a transcript amplification of 214 bp. (C) Western analysis of Mfrn1, porin, and tubulin in cytosol, mitochondria, and total bone marrow isolated from mice with the specified genotypes. (D) Bar graph of spleen weight/total weight of mice with the noted genotypes. (E). Hematoxylin and eosin–stained sections of spleen from Mfrn1+/+ mice and Mx-Cre–deleted Mfrn1−/− mice.

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