Tissue-specific expression of c-jun and junB during organogenesis in the mouse

Abstract

c-jun and junB are cellular genes related to the viral oncogene v-jun and encode members of the AP-1 transcription factor gene family. These genes have been implicated in the control of the G0/G1 transition in fibroblasts. Here, we have investigated the potential roles of c-jun and junB during fetal growth and organogenesis in the mouse by in situ hybridization analysis of their expression patterns. c-jun expression is detected throughout organogenesis, and transcripts are detected in many tissues, although in restricted cell populations within developing cartilage, gut and the central nervous system (CNS). In cartilage, c-jun expression is associated with rapidly proliferating perichondrial cells, but occurs in postmitotic motor neurones in the CNS. junB expression is initiated between 14.5 and 17.5 days of development, and is restricted to differentiating epidermal cells and endodermal gut epithelium. These data suggest that c-jun and junB have distinct, tissue-specific roles in cell proliferation and differentiation during fetal development.

The Wnt antagonist Dickkopf-1 is regulated by Bmp signaling and c-Jun and modulates programmed cell death

“…In the late limb bud, the developing joints represent another prominent site of co‐expression of Dkk‐1 and c‐ Jun . Interestingly, the domains of Bmp‐4, Dkk‐1 and c‐ Jun also overlap at other sites in the embryo, including the otic vesicle and branchial arches, where apoptosis plays a pivotal role to elaborate the shape of the corresponding structure (Wilkinson et al ., 1989; Sanz et al ., 1999; data not shown). This indicates that the molecular cascade for Bmp‐triggered apoptosis we propose (see below) is not limited to the developing limb but might be of general relevance during embryonic development.…”

MafB, a New Maf Family Transcription Activator That Can Associate with Maf and Fos but Not with Jun

“…The levels of expression of c-jun and c-fos are rapidly elevated by many growth-stimulatory signals (3). Unlike c-fos, however, c-jun and its related genes are known to be expressed to some extent in a wide variety of tissues in a tissueand stage-specific manner without cell growth stimuli (15,18,35,40,41,48). It is thus plausible that the expression of the Jun family proteins differentially affects the function of Maf and MafB proteins.…”

“…For instance, c-jun and junB are known to be immediate early genes whose expression is rapidly and transiently induced by cell growth-stimulatory signals (3,41,47), whereas the expression of junD is constitutive and is scarcely affected under the same conditions (15,18,40). In adult tissues and during embryogenesis, these jun family genes are expressed at different sites (15,18,35,40,48). In addition, their protein products have different biochemical and physiological properties.…”

YAP/Smad3 promotes pathological extracellular matrix microenviroment‐induced bladder smooth muscle proliferation in bladder fibrosis progression

“… 37 JUN is currently repeated to be involved in the embryonic brain development, cell‐cycle regulation, apoptosis, and axis formation. 38 , 39 , 40 Some studies have reported that the N‐terminal kinase JUN N‐terminal kinases (JNK) of JUN can activate the MAPK signaling pathway to regulate drug sensitivity and tumor resistance. 41 In our study, CUT and TAG sequencing and dual‐luciferase reporter assay demonstrated that Smad3 might inhibit the transcription of JUN which is contrary to the conclusions of some current studies.…”

“…JUN is a proto‐oncogene first discovered in the genome of avian sarcoma virus 17(ASV17) 37 . JUN is currently repeated to be involved in the embryonic brain development, cell‐cycle regulation, apoptosis, and axis formation 38–40 . Some studies have reported that the N‐terminal kinase JUN N‐terminal kinases (JNK) of JUN can activate the MAPK signaling pathway to regulate drug sensitivity and tumor resistance 41 .…”