Human ZCCHC12 activates AP-1 and CREB signaling as a transcriptional co-activator

Li, Hong; Liu, Qian; Hu, Xiang; Du, Feng; Xiang, Sheng; He, Zhicheng; Hu, Xingwang; Zhou, Jianlin; Ding, Xiaofeng; Zhou, Chang; Zhang, Jian

doi:10.1093/abbs/gmp042

Cited by 16 publications

(11 citation statements)

References 32 publications

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“…Interestingly, expression in the midbrain spans the entire neural tube from ventral to dorsal (Fig 1I and 1J). Although previous reports suggested that Sizn1 (Zcchc12) is expressed broadly within the neuroepithelium of the forebrain, diencephalon, midbrain and hindbrain of E10.5 mouse embryos (Li et al, 2009), our data indicate there is spatially and temporally restricted Sizn1 gene expression in the developing embryonic mouse brain.…”

Section: Resultscontrasting

confidence: 97%

XLMR candidate mouse gene, Zcchc12 (Sizn1) is a novel marker of Cajal–Retzius cells

Cho

Lim

Golden

2011

Gene Expression Patterns

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Sizn1 (Zcchc12) is a transcriptional co-activator that positively modulates BMP (Bone Morphogenic Protein) signaling through its interaction with Smad family members and CBP. We have demonstrated a role for Sizn1 in basal forebrain cholinergic neuron specific gene expression. Furthermore, mutations in SIZN1 have been associated with X-linked mental retardation. Given the defined role of SIZN1 in mental retardation, knowing its complete forebrain expression pattern is essential to further elucidating its role in cognition. To better define the dynamic expression pattern of Sizn1 during forebrain development, we investigated its expression in mouse brain development from embryonic day 8.0 (E8.0) to adult. We found that Sizn1 is primarily restricted to the ventral forebrain including the medial ganglionic eminence, the septum, amygdala, and striatum. In addition, Sizn1 expression is detected in the cortical hem and Pallial-subpallial boundary (PSB; anti-hem); both sources of Cajal-Retzius cells. Sizn1 expression in the dorsal forebrain is restricted to a subset of cells in the marginal zone that also express Reln, indicative of Cajal-Retzius cells. These data provide novel information on brain regions and cell types that express Sizn1, facilitating further investigations into the function of Sizn1 in both development and the pathogenesis of mental retardation.

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Section: Resultscontrasting

confidence: 97%

XLMR candidate mouse gene, Zcchc12 (Sizn1) is a novel marker of Cajal–Retzius cells

Cho

Lim

Golden

2011

Gene Expression Patterns

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“…The nuclear localization signal (NLS) of PNMA7A plays an important role for protein translocation to nucleus where PNMA7A was reported to function as transcriptional activator by interacting with Smad1 and CBP in BMP mediated cell signalling [25]. In addition, PNMA7A was found to activate AP-1 and CREB, and interacts with C-Jun through its nuclear targeting function [67]. [70,71], providing further evidence to support that ZCCHC12…”

Section: Accepted Manuscriptmentioning

confidence: 87%

“…Other than BMP cell signalling, PNMA7A was identified as transcriptional co-activator that interacts with c-Jun and activates AP-1 and CREB signalling [67]. Like many members of PNMA family, PNMA7A was found to be predominantly expressed in mouse brain,…”

Section: Interaction With Transcription Factors and Growth Factorsmentioning

confidence: 99%

PNMA family: Protein interaction network and cell signalling pathways implicated in cancer and apoptosis

Pang

Lahiri

Poh

et al. 2018

Cellular Signalling

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Paraneoplastic Ma Family (PNMA) comprises a growing number of family members which share relatively conserved protein sequences encoded by the human genome and is localized to several human chromosomes, including the X-chromosome. Based on sequence analysis, PNMA family members share sequence homology to the Gag protein of LTR retrotransposon, and several family members with aberrant protein expressions have been reported to be closely associated with the human Paraneoplastic Disorder (PND). In addition, gene mutations of specific members of PNMA family are known to be associated with human mental retardation or 3-M syndrome consisting of restrictive post-natal growth or dwarfism, and development of skeletal abnormalities. Other than sequence homology, the physiological function of many members in this family remains unclear. However, several members of this family have been characterized, including cell signalling events mediated by these proteins that are associated with apoptosis, and cancer in different cell types. Furthermore, while certain PNMA family members show restricted gene expression in the human brain and testis, other PNMA family members exhibit broader gene expression or preferential and selective protein interaction profiles, suggesting functional divergence within the family. Functional analysis of some members of this family have identified protein domains that are required for subcellular localization, protein-protein interactions, and cell signalling events which are the focus of this review paper.

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“…Each path held three classes of genes: those with expression that peaked at early, in the middle, or later in the trajectory ( Fig 4D-E ). Path 1, which is defined by cells from SC1_ B1, starts with an expression of limb mesenchyme (high Prrx2 (Leussink et al 1995), Zcchc12 (Li et al 2009)), then expression of Col1a2 and Bmp2 peaks in the middle stage, and it ends in the high Gdf5 and high Sfrp2 state. Epoch predicted that the major regulators of the first stage are Maf, a known regulator of chondrocyte differentiation (MacLean et al 2003), Isl1 (Yang et al 2006), Ebf1 and Sox4, detected in IZ with unknown mechanism (Jenner et al 2014; Bhattaram et al 2014) and Lin28b, an indicator of embryonic to adult transitioning (Zhang et al 2016) ( Fig 4D ).…”

Section: Resultsmentioning

confidence: 99%

A single cell transcriptional atlas of early synovial joint development

Bian

Cheng

Wilson

et al. 2019

Preprint

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42 43 2 SUMMARY 44 45 Synovial joint development begins with the formation of the interzone, a region of condensed 46 mesenchymal cells at the site of the prospective joint. Recently, lineage tracing strategies have 47 55 transcriptional atlas will serve as a resource for the community to uncover transcriptional 56 programs and cell interactions that regulate synovial joint development. 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 100 to laser-capture micro-dissected regions of the interzone (Jenner et al. 2014). While these 101 investigations have yielded new insights into the genetic programs underpinning limb and joint 102 morphogenesis, they provide limited resolution of the expression states for individual cell types 103 due to the heterogenous nature of the samples profiled. With the advent of single cell profiling, it 104 is now possible to detect transient populations of cells, to reconstruct developmental 105 4 transcriptional programs, and to identity new cell populations (Guo et al. 2010; Kumar et al. 106 2017). For example, Feng et al revealed molecular signatures and lineage trajectories of an 107 interzone related Lgr5 + population in the murine E14.5 knee joint that contributes to the 108 formation of cruciate ligaments, synovial membrane, and articular chondrocytes (Feng et al. 109 2019). 110 111 Here, we applied single-cell RNA-sequencing on Gdf5-lineage cells of the murine hindlimb to 112 determine the transcriptional programs of early synovial joint development. In contrast to the 113 recent study of Feng et al 2019, which focused on lineage divergence of a specific Lrg5 + 114interzone population, we sought to characterize formation of the entire IZ and to discover the 115 extent to which heterogeneity in the nascent interzone is resolved into the distinct lineages that 116 are apparent later at cavitation. Therefore, we sequenced Gdf5-lineage cells from the 117 presumptive joint of the hindlimb from E12.5 (prior to frank IZ formation) through E15.5 118 (coinciding with cavitation). We combined computational analytics and in situ hybridization to 119 infer the lineage relationships of joint progenitors and to identify the combinatorial transcriptional 120 programs that mediate the elaboration of the interzone into the major synovial joint lineages. We 121 found that early Gdf5-lineage enriched cells consist of sub-populations with chondrogenic or 122 fibrous-lineage bias. Furthermore, we discovered within the chondrogenic-biased population 123 were two distinct sub-populations that followed similar trajectories to de-differentiate into IZ 124 cells, supporting a model of regionally and temporally complex IZ specification (Shwartz et al. 125 2016). To aid the community in discovering additional transcriptional programs and in inferring 126 cell interactions that contribute to synovial joint development, we have made this data freely and 127 easily accessible with a web application at http://www.cahanlab.org/resources/joint_ontogeny. 128 129 Results 130 131 Gdf5Cre + cells in the hind limb ...

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Human ZCCHC12 activates AP-1 and CREB signaling as a transcriptional co-activator

Cited by 16 publications

References 32 publications

XLMR candidate mouse gene, Zcchc12 (Sizn1) is a novel marker of Cajal–Retzius cells

XLMR candidate mouse gene, Zcchc12 (Sizn1) is a novel marker of Cajal–Retzius cells

PNMA family: Protein interaction network and cell signalling pathways implicated in cancer and apoptosis

A single cell transcriptional atlas of early synovial joint development

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