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An amylase/cre transgene marks the whole endoderm but the primordia of liver and ventral pancreas
Author(s) -
Kockel Liliana,
Strom Alessandra,
Delacour Alexandra,
Népote Virginie,
Hagenbüchle Otto,
Wellauer Peter K.,
Herrera Pedro L.
Publication year - 2006
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/dvg.20206
Subject(s) - endoderm , biology , transgene , pancreas , genetically modified mouse , primordium , embryonic stem cell , cre recombinase , pdx1 , microbiology and biotechnology , endocrinology , transcription factor , gene , genetics
Mice bearing a Cre‐encoding transgene driven by a compound [ SV40 small t antigen/mouse α‐ amylase‐2 ] promoter expressed the recombinase at early developmental stages broadly in the embryonic endoderm before the pancreas and lungs begin to outgrow, but not in other germ layers, as determined indirectly by β‐galactosidase and YFP reporter activity, indicating that the transgene is in fact an endodermic marker. Interestingly, the liver and ventral pancreas were excluded from this expression pattern, denoting that the chimerical α‐ amylase‐2 promoter was not active in the anterior leading edge of the endoderm (the presumptive region from which liver and ventral pancreas form). These transgenics thus confirm, among other findings, that dorsal and ventral pancreatic primordia have different intrinsic transcriptional capabilities. In conclusion, we have generated a new transgenic mouse that should be useful to target endoderm at early stages, without affecting the liver or ventral pancreas before embryonic day E12.5. genesis 44:287–296, 2006. © 2006 Wiley‐Liss, Inc.