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The Journal of Neuroscience, November 19, 2003, 23(33):10568-10576

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Development/Plasticity/Repair
Tlx Controls Proliferation and Patterning of Lateral Telencephalic Progenitor Domains

Jan M. Stenman,^1,2 Bei Wang,¹ and Kenneth Campbell¹

¹Division of Developmental Biology, Children's Hospital Research Foundation, Cincinnati, Ohio 45229-3039, and ²Wallenberg Neuroscience Center, Division of Neurobiology, Lund University, S-221 84 Lund, Sweden

We showed previously that the orphan nuclear receptor Tlx is required for the correct establishment of the pallio-subpallial boundary. Loss of Tlx results in a dorsal expansion of ventral markers (e.g., the homeodomain protein GSH2) into the ventralmost pallial region, i.e., the ventral pallium. We also observed a disproportionate reduction in the size of the Tlx mutant lateral ganglionic eminence (LGE) from embryonic day 14.5 onward. Here we show that this reduction is caused, at least in large part, by a proliferation defect. Interestingly, in Tlx mutants, the LGE derivatives are differentially affected. Although the development of the Tlx mutant striatum is compromised, an apparently normal number of olfactory bulb interneurons are observed. Consistent with this observation, we found that Tlx is required for the normal establishment of the ventral LGE that gives rise to striatal projection neurons. This domain is reduced by the dorsal and ventral expansion of molecular markers normally confined to progenitor domains flanking the ventral LGE. Finally, we investigated possible genetic interactions between Gsh2 and Tlx in lateral telencephalic development. Our results show that, although Gsh2 and Tlx have additive effects on striatal development, they differentially regulate the establishment of ventral pallial identity.

Key words: GSH2; Neurogenin2; NR2E1; striatum; subpallium; tailless; ventral pallium; ventral LGE; dorsal LGE; Dbx1; SFRP2; NKX6.2; Er81; ISL1

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Received July 31, 2003; revised September 11, 2003; accepted September 30, 2003.

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