Premium
Genes dependent on zebrafish cyclops function identified by AFLP differential gene expression screen
Author(s) -
Rubinstein Amy L.,
Lee Danny,
Luo Rushu,
Henion Paul D.,
Halpern Marnie E.
Publication year - 2000
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/(sici)1526-968x(200001)26:1<86::aid-gene11>3.0.co;2-q
Subject(s) - biology , zebrafish , somitogenesis , mutant , calreticulin , gene , microbiology and biotechnology , gastrulation , genetics , complementary dna , somite , embryogenesis , endoplasmic reticulum
Summary: Zebrafish cyclops ( cyc ) encodes a Transforming Growth Factor β (TGFβ) signaling factor closely related to mouse Nodal. By comparing amplified fragment length polymorphisms (AFLP) from cyc mutant and wild‐type cDNA pools, we devised a differential gene expression screen to isolate genes whose expression is dependent on Cyc signaling. We report two genes not previously described in the zebrafish that were identified using this approach. The first gene, crestin , is expressed predominantly in premigratory and migrating neural crest cells during somitogenesis stages. crestin expression is reduced in cyc mutants initially but recovers by late somitogenesis. The second gene encodes the zebrafish homologue of the calcium‐binding protein, calreticulin. Zebrafish calreticulin is highly expressed in the hatching gland and in the floor plate, tissues that are affected in cyc mutants. During gastrulation, calreticulin transcripts are found in the dorsal mesendoderm, in the same cells that express the cyc gene. Expression is reduced in cyc mutants and is abolished by the one ‐ eyed pinhead ( oep ) mutation that is presumed to prevent Nodal signaling. The identification of calreticulin suggests that a differential screen between wild‐type and mutant cDNA is a useful approach to reveal regulation of unexpected gene expression in response to cellular signals. genesis 26:86–97, 2000. © 2000 Wiley‐Liss, Inc.