Foxg1 Regulate The Development Of The Pituitary Gland

The Pituitary gland is an important endocrine gland,which located in the sphenoid bone called the sella turcica,at the base of the skull.The pituitary gland is anatomically and functionally subdivided into two different components,the adenohypophysis,including the anterior and intermediate lobes,and neurohypophysis,also known as the posterior lobe.The neurohypophysis is generated from the embryonic neuroderm,only stores and releases the endocrine hormones produced by supraoptic nucleus and paraventricular nucleus of hypothalamus,while the adenohypophysis produces and releases five distinct hormones.These endocrine hormones enter the blood circulation via pituitary portal system and target their distinct organs/cells to regulate homeostasis,metabolism,growth,reproduction,and lactation.The disfunction of pituitary often leads to abnormalities of the individual,congenital pituitary dysplasia often causes adolescent dysplasia/adolescent dysplasia,microphthalmia/anophthalmia,corpus callosum dysplasia,and optical-septal dysplasia,and the anterior lobe obtained a smaller size,posterior lobe ectopic.Hence,it is of great significance to explore the mechanism underlying the development of the adenohypophysis.Foxg1(brain factor1,BF1),a telencephalo-specific transcription factor,is involved in the regulation of telencephalic development and the maintenance of telencephalic function in both embryo and in adulthood.Previous studies have shown that Foxg1 plays a critical role in the proliferation,differentiation,migration,localization and apoptosis of neuronal cells.The deficiency of Foxg1 gene leads to FOXG1 syndrome,which is mainly manifested as microcephaly,corpus callosum hypoplasia,mental retardation,language loss,anxiety ect.Recent study has revealed that Foxg1 is also expressed in the adenohypophysis primordium.Since microcephaly,corpus callosum dysplasia and mental retardation is also resulted from pituitary dysfunction.However,the role of Foxg1 in the development of the pituitary gland remains unrevealed.Here,in this study,we found the overall thickness of the pituitary gland in Foxg1 knockout mice is thinner than their littermates.The number of all 5 kinds of hormone-release cells was significantly reduced at E18.5.The expression of key regulators in pituitary development such as Pax6,Lhx3,Six6 were reduced as early as E12.5.Finally,the proliferation of the pituitary generator was severaly impaired.Our work provides new insight into cellular basis of the FOXG1 sydrome.