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Differential expression pattern of ZAC in developing mouse and human pancreas
Xiaoyu Du1, Marylene Rousseau, Houria Ounissi-Benkalha
1Division of Pediatric Endocrinology, McGill University Health Centre Research Institute, Children's Hospital, 4060 St. Catherine west, PT-414, Montreal, QC, H3Z 2Z3, Canada.
Journal of Molecular Histology
|February 10, 2011
Summary
Transient neonatal diabetes mellitus (TNDM) may involve ZAC gene dosage. ZAC is expressed in human fetal beta-cells, but not mouse mesenchyme, explaining TNDM severity differences.
Area of Science:
- Developmental Biology
- Genetics
- Endocrinology
Background:
- ZAC is a transcription factor implicated in transient neonatal diabetes mellitus (TNDM).
- TNDM is linked to impaired beta-cell development, potentially due to ZAC gene dosage issues.
- ZAC/Zac1 expression patterns in the developing pancreas are largely unknown.
Purpose of the Study:
- To investigate ZAC/Zac1 expression in developing mouse and human pancreata.
- To elucidate the role of ZAC/Zac1 in pancreatic development and TNDM pathogenesis.
Main Methods:
- Real-time PCR
- Dual in situ hybridization
- Immunofluorescence
Main Results:
- Pancreatic ZAC/Zac1 expression declined significantly during development in both species.
- Mouse embryonic Zac1 showed predominant mesenchymal expression.
- Human fetal ZAC was specifically expressed in pancreatic islets, particularly beta-cells.
Conclusions:
- ZAC/Zac1 exhibit distinct expression patterns in developing mouse and human pancreata.
- Specific ZAC expression in human fetal beta-cells supports its role in TNDM.
- Differential expression may explain milder phenotypes in mouse models of ZAC duplication.
