MYB81, a microspore‐specific GAMYB transcription factor, promotes pollen mitosis I and cell lineage formation in Arabidopsis

AbstractDevelopmental outcomes are shaped by the interplay between intrinsic and external factors. The production of stomata—essential pores for gas exchange in plants—is extremely plastic and offers an excellent system to study this interplay at the cell lineage level. For plants, light is a key external cue, and it promotes stomatal development and the accumulation of the master stomatal regulator SPEECHLESS (SPCH). However, how light signals are relayed to influence SPCH remains unknown. Here, we show that the light-regulated transcription factor ELONGATED HYPOCOTYL 5 (HY5), a critical regulator for photomorphogenic growth, is present in inner mesophyll cells and directly binds and activates STOMAGEN. STOMAGEN, the mesophyll-derived secreted peptide, in turn stabilizes SPCH in the epidermis, leading to enhanced stomatal production. Our work identifies a molecular link between light signaling and stomatal development that spans two tissue layers and highlights how an environmental signaling factor may coordinate growth across tissue types.

Download Full-text

RUNX1 maintains the identity of the fetal ovary through an interplay with FOXL2

Nature Communications ◽

10.1038/s41467-019-13060-1 ◽

2019 ◽

Vol 10 (1) ◽

Cited By ~ 8

Author(s):

Barbara Nicol ◽

Sara A. Grimm ◽

Frédéric Chalmel ◽

Estelle Lecluze ◽

Maëlle Pannetier ◽

...

Keyword(s):

Transcription Factor ◽

Granulosa Cell ◽

Sertoli Cells ◽

Transcriptional Control ◽

Cell Lineage ◽

Supporting Cell ◽

Supporting Cells ◽

Fate Specification ◽

Fetal Ovary

Abstract Sex determination of the gonads begins with fate specification of gonadal supporting cells into either ovarian pre-granulosa cells or testicular Sertoli cells. This fate specification hinges on a balance of transcriptional control. Here we report that expression of the transcription factor RUNX1 is enriched in the fetal ovary in rainbow trout, turtle, mouse, goat, and human. In the mouse, RUNX1 marks the supporting cell lineage and becomes pre-granulosa cell-specific as the gonads differentiate. RUNX1 plays complementary/redundant roles with FOXL2 to maintain fetal granulosa cell identity and combined loss of RUNX1 and FOXL2 results in masculinization of fetal ovaries. At the chromatin level, RUNX1 occupancy overlaps partially with FOXL2 occupancy in the fetal ovary, suggesting that RUNX1 and FOXL2 target common sets of genes. These findings identify RUNX1, with an ovary-biased expression pattern conserved across species, as a regulator in securing the identity of ovarian-supporting cells and the ovary.

Download Full-text

Transcription factor B cell lineage-specific activator protein regulates the gene for human X-box binding protein 1.

Journal of Experimental Medicine ◽

10.1084/jem.183.2.393 ◽

1996 ◽

Vol 183 (2) ◽

pp. 393-401 ◽

Cited By ~ 123

Author(s):

A M Reimold ◽

P D Ponath ◽

Y S Li ◽

R R Hardy ◽

C S David ◽

...

Keyword(s):

Transcription Factor ◽

B Cell ◽

Cell Lines ◽

Binding Protein ◽

Cell Lineage ◽

Regulatory Elements ◽

Target Sequence ◽

Consensus Binding Site ◽

Mobility Shift ◽

Activator Protein

The transcription factor human X-box binding protein 1 (hXBP-1) is a basic region-leucine zipper protein implicated in the regulation of major histocompatibility complex class II gene expression as well as in exocrine gland and skeletal development. Multiple regulatory elements in the hXBP-1 promoter lie 3' to the transcription start site, including the hX2 site, whose core sequence is an AP-1-like element identical to the hXBP-1 target sequence in the HLA-DRA promoter. One complex identified by electrophoretic mobility shift assay (EMSA), complex 3, was previously shown to protect the hX2 site and more 3' bases. Sequence analysis now shows that this region contains a consensus binding site for transcription factor BSAP (B cell lineage-specific activator protein). Complex 3 and BSAP have identical cell-type specificities, as they are found only in pre-B and mature B cell lines. In EMSAs, BSAP antibody specifically recognized complex 3, and in vitro translated BSAP could bind to an hXBP promoter fragment. Cotransfections using an hXBP-1 reporter construct indicated that BSAP downregulates the hXBP-1 promoter. The highest levels of hXBP-1 mRNA were found when BSAP was not expressed, in pre-Pro-B cells and in plasma cell lines. In addition, hXBP-1 and BSAP levels were inversely correlated along the early stages of B cell development. In the regulation of the hXBP-1 promoter, a strong positive transcriptional influence at the hX2 site is opposed by the downregulatory actions of BSAP.

Download Full-text

Transcription Factor PAX6 (Paired Box 6) Controls Limbal Stem Cell Lineage in Development and Disease

Journal of Biological Chemistry ◽

10.1074/jbc.m115.662940 ◽

2015 ◽

Vol 290 (33) ◽

pp. 20448-20454 ◽

Cited By ~ 29

Author(s):

Gen Li ◽

Fan Xu ◽

Jie Zhu ◽

Michal Krawczyk ◽

Ying Zhang ◽

...

Keyword(s):

Transcription Factor ◽

Stem Cell ◽

Cell Lineage ◽

Stem Cell Lineage ◽

Limbal Stem Cell

Download Full-text

The ETS oncogene family transcription factor FEV identifies serotonin-producing cells in normal and neoplastic small intestine

Endocrine Related Cancer ◽

10.1677/erc-09-0243 ◽

2010 ◽

Vol 17 (1) ◽

pp. 283-291 ◽

Cited By ~ 10

Author(s):

Yu-cheng Wang ◽

Marlene B Zuraek ◽

Yasuhiro Kosaka ◽

Yasuharu Ota ◽

Michael S German ◽

...

Keyword(s):

Transcription Factor ◽

Small Intestine ◽

Cell Lineage ◽

Lineage Tracing ◽

Serotonin Neurons ◽

In The Wild ◽

Normal Human ◽

Node Metastases ◽

Novel Target

Neuroendocrine (NE) or carcinoid tumors of the small intestine (SI) frequently metastasize and produce the hormone serotonin, causing significant morbidity and mortality. A member of the ETS oncogene family of transcription factors, Fev, acts with the homeodomain transcription factor Nkx2.2 in the development of serotonin neurons in mice. In this study, we investigated the role of Fev in normal and neoplastic SI. In NE tumors (NETs) of the SI, serotonin stimulates tumor growth and causes debilitating symptoms, such as diarrhea, flushing, wheezing, and right-sided valvular heart disease (i.e. carcinoid syndrome). Compared with those in the matched normal human SI, FEV expression levels were significantly elevated in primary NETs (20-fold, P<0.0001), lymph node metastases (35-fold, P=0.004), and NET liver metastases (22-fold, P<0.0001) resected from patients with serotonin excess. Fev is expressed in the wild type but not in Nkx2.2 (−/−) mouse SI, in which cells producing serotonin are absent. Using recombination-based cell lineage tracing, we found that FEV-positive cells give rise to serotonin-producing cells in the SI. In Fev (−/−) mouse SI, we observed no difference in the number of cells producing serotonin or other hormones. We conclude that FEV expression identifies serotonin-producing cells in normal and neoplastic SI and is a novel target for diagnosis of patients with NETs of the SI.

Download Full-text

Targeted Overexpression of the Transcription Factor XBP-1 in B Cells Promotes Plasma Cell and Lymphoplasmacytic Neoplasms in Transgenic Mice.

Blood ◽

10.1182/blood.v106.11.359.359 ◽

2005 ◽

Vol 106 (11) ◽

pp. 359-359 ◽

Cited By ~ 2

Author(s):

Ruben D. Carrasco ◽

Kumar Sukhdeo ◽

Marina Protopopova ◽

Masha German ◽

Joel Henderson ◽

...

Keyword(s):

Transcription Factor ◽

B Cells ◽

Growth Factor ◽

B Cell ◽

Signaling Pathways ◽

Plasma Cell ◽

Rna Processing ◽

Cell Lineage ◽

Growth Factor Signaling ◽

Factor X

Abstract The transcription factor X-box binding protein-1 (XBP-1) plays critical roles in the unfolded protein response (UPR), the differentiation of plasma cells, and the regulation of growth factor signaling pathways. XBP-1 is subject to regulation by alternative RNA processing producing XBP-1-spliced (S) and -unspliced (U) mRNAs encoding proteins with identical DNA-binding and bZIP domains yet distinct C-terminal transactivation domains. The weaker transactivation potential of XBP-1(U) has prompted speculation that it may influence XBP-1(S) activity as a transdominant mutant. While elevated XBP-1 expression has been reported in transformed cells, the relative ratios of these XBP-1 isoforms and associated physiological relevance in cancer are uncertain. Here, we assessed the differential impact of enforced XBP-1(S) versus XBP-1(U) transgene expression in the B cell lineage. Both transgenes elicited early onset antibody-dependent autoimmune disease characterized by elevated levels of serum immunoglobulin (Ig) and IL-6 production, increased numbers of marginal zone and mature follicular B cells in the spleen, and expanded mature B cell populations in the bone marrow. Notably, aged XBP-1(S) mice developed clonal plasma cell expansions, culminating in the human-equivalent of Monoclonal Gammopathy of Undetermined Significance (MGUS) or Multiple Myeloma (MM). Conversely, XBP-1(U) mice develop multi-organ lymphoplasmacytic infiltrates and, with advancing age, succumb to neoplasms resembling human Lymphoplasmacytic Lymphoma/Waldenstrom’s Macroglobulinemia (LPL/WM). These unanticipated genetic observations in the mouse were translated to human disease with documentation of elevated levels of XBP-1(S) in MM and XBP-1(U) in LPL/WM. Together, these results indicate that imbalances in XBP-1(S) and XBP-1(U) alters B cell lineage homeostasis and can drive two distinct types of lymphoplasmacytic neoplasms in vivo. The findings of this study, together with the known capacity of XBP-1 to regulate various cancer-relevant growth factor signaling pathways, predicts that epigenetic dysregulation of alternate XBP-1 RNA processing can promote age-associated B cell malignancies in humans.

Download Full-text

Transcription factor GATA-3 is required for development of the T-cell lineage

Nature ◽

10.1038/384474a0 ◽

1996 ◽

Vol 384 (6608) ◽

pp. 474-478 ◽

Cited By ~ 427

Author(s):

Chao-Nan Ting ◽

Marilyn C. Olson ◽

Kevin P. Barton ◽

Jeffrey M. Leiden

Keyword(s):

Transcription Factor ◽

T Cell ◽

Cell Lineage

Download Full-text

Requirement of a Myocardin-Related Transcription Factor for Development of Mammary Myoepithelial Cells

Molecular and Cellular Biology ◽

10.1128/mcb.00211-06 ◽

2006 ◽

Vol 26 (15) ◽

pp. 5797-5808 ◽

Cited By ~ 118

Author(s):

Shijie Li ◽

Shurong Chang ◽

Xiaoxia Qi ◽

James A. Richardson ◽

Eric N. Olson

Keyword(s):

Transcription Factor ◽

Smooth Muscle ◽

Myoepithelial Cell ◽

Serum Response Factor ◽

Cell Lineage ◽

Myoepithelial Cells ◽

Embryonic Cell ◽

Loss Of Function ◽

Muscle Gene Expression ◽

Related Transcription Factor

ABSTRACT The mammary gland consists of a branched ductal system comprised of milk-producing epithelial cells that form ductile tubules surrounded by a myoepithelial cell layer that provides contractility required for milk ejection. Myoepithelial cells bear a striking resemblance to smooth muscle cells, but they are derived from a different embryonic cell lineage, and little is known of the mechanisms that control their differentiation. Members of the myocardin family of transcriptional coactivators cooperate with serum response factor to activate smooth muscle gene expression. We show that female mice homozygous for a loss-of-function mutation of the myocardin-related transcription factor A (MRTF-A) gene are unable to effectively nurse their offspring due to a failure in maintenance of the differentiated state of mammary myoepithelial cells during lactation, resulting in apoptosis of this cell population, a consequent inability to release milk, and premature involution. The phenotype of MRTF-A mutant mice reveals a specific and essential role for MRTF-A in mammary myoepithelial cell differentiation and points to commonalities in the transcriptional mechanisms that control differentiation of smooth muscle and myoepithelial cells.

Download Full-text