Gli2, a zinc-finger transcription factor, is a key component of the Sonic Hedgehog (Shh) signaling pathway [1,2]. This pathway is vital in multiple biological processes such as development, cell differentiation, and tissue homeostasis. Gli2 acts as an intermediary in Shh signaling, which has significant importance in embryonic development, dorsoventral patterning, and axon guidance [3]. Genetic models, like gene knockout (KO) mouse models, have been crucial in studying Gli2.

Gli2 mutant mice have hypoplastic anterior and absent posterior pituitary glands, indicating its role in pituitary development [1]. In these mice, the phenotype often includes growth hormone (GH) deficiency, a small anterior pituitary lobe, an ectopic/undescended posterior pituitary lobe, and postaxial polydactyly [1]. In the context of thalamocortical projection guidance, Gli2-mediated Shh signaling is essential. In Gli2 knockout mouse embryos, thalamocortical axons follow incorrect trajectories, likely due to alterations in the Robo/Slit signaling mechanism [3].

In conclusion, Gli2 is essential for normal development, especially in pituitary and neural development as revealed by KO mouse models. Understanding Gli2's function can provide insights into diseases related to pituitary dysfunction and neural developmental disorders.

References:

1. Arnhold, Ivo J P, França, Marcela M, Carvalho, Luciani R, Mendonca, Berenice B, Jorge, Alexander A L. 2015. Role of GLI2 in hypopituitarism phenotype. In Journal of molecular endocrinology, 54, R141-50. doi:10.1530/JME-15-0009. https://pubmed.ncbi.nlm.nih.gov/25878059/

2. Cohen, Laurie E. . GLI2 mutations as a cause of hypopituitarism. In Pediatric endocrinology reviews : PER, 9, 706-9. doi:. https://pubmed.ncbi.nlm.nih.gov/23304807/

3. Callejas-Marin, Antuca, Moreno-Bravo, Juan Antonio, Company, Verónica, Martínez, Salvador, Puelles, Eduardo. 2022. Gli2-Mediated Shh Signaling Is Required for Thalamocortical Projection Guidance. In Frontiers in neuroanatomy, 16, 830758. doi:10.3389/fnana.2022.830758. https://pubmed.ncbi.nlm.nih.gov/35221935/