Islet1 and Islet2 have equivalent abilities to promote motoneuron formation and to specify motoneuron subtype identity
- Hutchinson, S.A., and Eisen, J.S.
- Development (Cambridge, England) 133(11): 2137-2147 (Journal)
- Registered Authors
- Eisen, Judith S.
- Primary motoneuron, Secondary motoneuron, LIM homeodomain, Interneuron, Spinal motoneuron, pMN domain, Zebrafish
- MeSH Terms
- Cell Differentiation*
- Gene Expression Regulation, Developmental
- Homeodomain Proteins/genetics
- Homeodomain Proteins/metabolism*
- LIM-Homeodomain Proteins
- Motor Neurons/cytology*
- Motor Neurons/metabolism*
- Nerve Tissue Proteins/genetics
- Nerve Tissue Proteins/metabolism*
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- 16672347 Full text @ Development
Hutchinson, S.A., and Eisen, J.S. (2006) Islet1 and Islet2 have equivalent abilities to promote motoneuron formation and to specify motoneuron subtype identity. Development (Cambridge, England). 133(11):2137-2147.
The expression of LIM homeobox genes islet1 and islet2 is tightly regulated during development of zebrafish primary motoneurons. All primary motoneurons express islet1 around the time they exit the cell cycle. By the time primary motoneurons undergo axogenesis, specific subtypes express islet1, whereas other subtypes express islet2, suggesting that these two genes have different functions. Here, we show that Islet1 is required for formation of zebrafish primary motoneurons; in the absence of Islet1, primary motoneurons are missing and there is an apparent increase in some types of ventral interneurons. We also provide evidence that Islet2 can substitute for Islet1 during primary motoneuron formation. Surprisingly, our results demonstrate that despite the motoneuron subtype-specific expression patterns of Islet1 and Islet2, the differences between the Islet1 and Islet2 proteins are not important for specification of the different primary motoneuron subtypes. Thus, primary motoneuron subtypes are likely to be specified by factors that act in parallel to or upstream of islet1 and islet2.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes