Ch. Wen et al., spr-2, a suppressor of the egg-laying defect caused by loss of sel-12 presenilin in Caenorhabditis elegans, is a member of the SET protein subfamily, P NAS US, 97(26), 2000, pp. 14524-14529
Citations number
39
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Presenilin plays critical roles in the genesis of Alzheimer's disease and i
n UN-12/Notch signaling during development. Here, we describe a screen far
genes that influence presenilin level or activity in Caenorhabditis elegans
. We identified four spr (suppressor of presenilin) genes by reverting the
egg-laying defective phenotype caused by a null allele of the sel-12 presen
ilin gene. We analyzed the spr-2 gene in some detail. We show that loss of
spr-2 activity suppresses the egg-laying defective phenotype of different s
el-12 alleles and re quires activity of the hop-1 presenilin gene, suggesti
ng that suppression is accomplished by elevating presenilin activity rather
than by bypassing the need for presenilin activity. We also show that SPR-
2 is a nuclear protein and is a member of a protein subfamily that includes
human SET, which has been identified in numerous different biochemical ass
ays and at translocation breakpoints associated with a subtype of acute mye
loid leukemia.