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Blood, Vol. 94 No. 2 (July 15), 1999:
pp. 818-824
Expression of the Fanconi Anemia Group A Gene (Fanca)
During Mouse Embryogenesis
Radwan Abu-Issa,
Gregor Eichele, and
Hagop Youssoufian
From the Departments of Molecular and Human Genetics, Biochemistry,
and Medicine, and the Developmental Biology Program, Baylor College of
Medicine, Houston, TX.
About 80% of all cases of Fanconi anemia (FA) can be accounted for
by complementation groups A and C. To understand the relationship between these groups, we analyzed the expression pattern of the mouse
FA group-A gene (Fanca) during embryogenesis and compared it
with the known pattern of the group-C gene (Fancc). Northern analysis of RNA from mouse embryos at embryonic days 7, 11, 15, and 17 showed a predominant 4.5 kb band in all stages. By in situ hybridization, Fanca transcripts were found in the whisker
follicles, teeth, brain, retina, kidney, liver, and limbs. There was
also stage-specific variation in Fanca expression, particularly
within the developing whiskers and the brain. Some tissues known to
express Fancc (eg, gut) failed to show Fanca
expression. These observations show that (1) Fanca is under
both tissue- and stage-specific regulation in several tissues; (2) the
expression pattern of Fanca is consistent with the phenotype of
the human disease; and (3) Fanca expression is not necessarily
coupled to that of Fancc. The presence of distinct tissue
targets for FA genes suggests that some of the variability in the
clinical phenotype can be attributed to the complementation group assignment.
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