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Distinct fetal Ank-1 and Ank-2 related proteins and mRNAs in normal and
nb/nb mice
LL Peters, LC Turtzo, CS Birkenmeier and JE Barker
Jackson Laboratory, Bar Harbor, ME 04609.
Mice homozygous for the mutation normoblastosis (gene symbol nb on
chromosome 8) are deficient in erythroid ankyrin (ANK-1) and have a severe
hemolytic anemia throughout life. Characteristic of the disease is a
dramatic decrease in the level of expression of the Ank-1 gene (chromosome
8). The other major ankyrin transcript, brain ankyrin (Ank- 2 on chromosome
3) is expressed at normal levels in nb/nb mice. Surprisingly, nb/nb fetuses
have normal erythrocyte counts despite the decreased levels of Ank-1
transcripts. We previously hypothesized that fetal-specific ankyrin-related
proteins could exist in nb/nb fetuses to account for the lack of
detrimental effects of ANK-1 deficiency. In the present report, Western and
Northern blot analyses were performed on hematopoietic cells isolated from
nb/nb and +/+ fetuses. An ANK-1- related protein (165 Kd) in fetal
reticulocytes persisted in adult nb/nb but not in +/+ reticulocytes. An
Ank-1-related transcript of 5.5 kb was found in fetal reticulocytes. This
transcript appeared to be upregulated in nb/nb but not in +/+ adult
reticulocytes. A fetal- specific ANK-2-related protein (155 Kd) was present
in nb/nb and in +/+ fetal reticulocytes. Ank-2-related fetal liver mRNAs
were present during the time the liver was actively generating
erythrocytes. Neither the Ank-2-related transcripts nor the 155-Kd
ANK-2-related protein were found in +/+ or mutant adult reticulocytes. The
data indicate that (1) unique ankyrin-related proteins and mRNAs present in
fetal erythrocytes may stabilize the ankyrin-deficient nb/nb erythrocytes
and (2) adult nb/nb mice may upregulate fetal gene transcripts to
compensate for the ANK-1 deficiency.
Volume 81,
Issue 8,
pp. 2144-2149,
04/15/1993
Copyright © 1993 by The American Society of Hematology
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