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GATA2 functions in adrenal chromaffin cells
Author(s) -
WatanabeAsaka Tomomi,
Hayashi Moyuru,
Engel James Douglas,
Kawai Yoshiko,
Moriguchi Takashi
Publication year - 2020
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12795
Subject(s) - biology , catecholamine , gata2 , adrenal medulla , embryonic stem cell , adrenal gland , endocrinology , chromaffin cell , medicine , conditional gene knockout , microbiology and biotechnology , homeostasis , neural crest , phenotype , embryo , stem cell , genetics , haematopoiesis , gene
Catecholamine synthesized in the sympathoadrenal system, including sympathetic neurons and adrenal chromaffin cells, is vital for cardiovascular homeostasis. It has been reported that GATA2, a zinc finger transcription factor, is expressed in murine sympathoadrenal progenitor cells. However, a physiological role for GATA2 in adrenal chromaffin cells has not been established. In this study, we demonstrate that GATA2 is specifically expressed in adrenal chromaffin cells. We examined the consequences of Gata2 loss‐of‐function mutations, exploiting a Gata2 conditional knockout allele crossed to neural crest‐specific Wnt1‐Cre transgenic mice ( Gata2 NC‐CKO). The vast majority of Gata2 NC‐CKO embryos died by embryonic day 14.5 (e14.5) and exhibited a decrease in catecholamine‐producing adrenal chromaffin cells, implying that a potential catecholamine defect might lead to the observed embryonic lethality. When intercrossed pregnant dams were fed with synthetic adrenaline analogs, the lethality of the Gata2 NC‐CKO embryos was partially rescued, indicating that placental transfer of the adrenaline analogs complements the lethal catecholamine deficiency in the Gata2 NC‐CKO embryos. These results demonstrate that GATA2 participates in the development of neuroendocrine adrenaline biosynthesis, which is essential for fetal survival.