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LIM genes parcellate the embryonic amygdala and regulate its development

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84167

Remedios,  R
Research Group Physiology of Sensory Integration, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Remedios, R., Subramanian, L., & Tole, S. (2004). LIM genes parcellate the embryonic amygdala and regulate its development. Journal of Neuroscience, 24(31), 6986-6990. doi:10.1523/​JNEUROSCI.0001-04.2004.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-D811-D
Abstract
The mechanisms that regulate the development of the amygdaloid complex are as yet poorly understood. Here, we show that in the absence of the LIM-homeodomain (LIM-HD) gene Lhx2, a particular amygdaloid nucleus, the nucleus of the lateral olfactory tract (nLOT), is selectively disrupted. LIM family members are well suited for multiple roles in the development of complex structures because they participate in regulatory interactions that permit a diversity of function. To investigate the possible role for other LIM-HD genes as well as LIM-only (Lmo) genes in the developing amygdala, we examined their expression in the embryo. We show that amygdaloid nuclei upregulate distinct patterns of LIM gene expression from embryonic stages. This supports the hypothesis that LIM genes may participate in the mechanisms that control the development of the amygdala. The disruption of the nLOT in the Lhx2 mutant is the first evidence of a role for LIM-HD genes in the development of the amygdaloid complex. The combinatorial expression patterns of LIM genes suggest a comprehensive mechanism for patterning this structure.