scholarly journals Drosophila grain encodes a GATA transcription factor required for cell rearrangement during morphogenesis

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4867-4876 ◽  
Author(s):  
S. Brown ◽  
J. Castelli-Gair Hombria
Keyword(s):  
Factor Analysis ◽  
Transcription Factor ◽  
Cellular Level ◽  
Epithelial Morphogenesis ◽  
Loss Of Function ◽  
Cell Rearrangement ◽  
Gata Transcription Factor ◽  
Gata Transcription Factors ◽  
Genetic Mechanisms ◽  
Organ Shape

The genetic mechanisms controlling organ shape are largely unknown. We show that the Drosophila grain gene is required during development for shaping the adult legs and the larval posterior spiracles. Mutant legs are short and wide rather than long and thin, while the spiracles are flat instead of dome-shaped. We demonstrate that grain encodes the GATAc transcription factor. Analysis of loss-of-function mutations at the cellular level indicates that grain affects organ shape by locally controlling cell rearrangement. Ectopic grain expression causes major morphogenetic movements, resulting in the invagination of the posterior segments into the embryo. This is the first gene that has been shown to affect epithelial morphogenesis by controlling cell rearrangements, and suggests a novel function for GATA transcription factors.

The LARGE2-APO1/APO2 regulatory module controls panicle size and grain number in rice

2021 ◽  
Author(s):  
Luojiang Huang ◽  
Kai Hua ◽  
Ran Xu ◽  
Dali Zeng ◽  
Ruci Wang ◽  
...  
Keyword(s):  
Agronomic Traits ◽  
Loss Of Function ◽  
Grain Number ◽  
Hect Domain ◽  
Regulatory Module ◽  
Promising Target ◽  
Meristematic Activity ◽  
Positive Regulators ◽  
Genetic Mechanisms ◽  
Biochemical Analyses

Abstract Panicle size and grain number are important agronomic traits and influence grain yield in rice (Oryza sativa), but the molecular and genetic mechanisms underlying panicle size and grain number control remain largely unknown in crops. Here we report that LARGE2 encodes a HECT-domain E3 ubiquitin ligase OsUPL2 and regulates panicle size and grain number in rice. The loss of function large2 mutants produce large panicles with increased grain number, wide grains and leaves, and thick culms. LARGE2 regulates panicle size and grain number by repressing meristematic activity. LARGE2 is highly expressed in young panicles and grains. Biochemical analyses show that LARGE2 physically associates with ABERRANT PANICLE ORGANIZATION1 (APO1) and APO2, two positive regulators of panicle size and grain number, and modulates their stabilities. Genetic analyses support that LARGE2 functions with APO1 and APO2 in a common pathway to regulate panicle size and grain number. These findings reveal a novel genetic and molecular mechanism of the LARGE2-APO1/APO2 module-mediated control of panicle size and grain number in rice, suggesting that this module is a promising target for improving panicle size and grain number in crops.

scholarly journals SREB, a GATA Transcription Factor That Directs Disparate Fates in Blastomyces dermatitidis Including Morphogenesis and Siderophore Biosynthesis

2010 ◽  
Vol 6 (4) ◽  
pp. e1000846 ◽  
Author(s):  
Gregory M. Gauthier ◽  
Thomas D. Sullivan ◽  
Sergio S. Gallardo ◽  
T. Tristan Brandhorst ◽  
Amber J. Vanden Wymelenberg ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Blastomyces Dermatitidis ◽  
Siderophore Biosynthesis ◽  
Gata Transcription Factor

The vacuolar amino acid transport system is a novel, direct target of GATA transcription factors

2021 ◽  
Vol 85 (3) ◽  
pp. 587-599
Author(s):  
Akane Sato ◽  
Takumi Kimura ◽  
Kana Hondo ◽  
Miyuki Kawano-Kawada ◽  
Takayuki Sekito
Keyword(s):  
Transcription Factors ◽  
Amino Acid ◽  
Amino Acid Transport ◽  
Amino Acid Transporters ◽  
Acid Transport ◽  
Amino Acid Transport System ◽  
Gata Transcription Factor ◽  
Gata Transcription Factors ◽  
Acid Status ◽  
Direct Target

ABSTRACT In Saccharomyces cerevisiae, Avt4 exports neutral and basic amino acids from vacuoles. Previous studies have suggested that the GATA transcription factors, Gln3 and Gat1, which are key regulators that adapt cells in response to changes in amino acid status, are involved in the AVT4 transcription. Here, we show that mutations in the putative GATA-binding sites of the AVT4 promoter reduced AVT4 expression. Consistently, a chromatin immunoprecipitation (ChIP) assay revealed that Gat1-Myc13 binds to the AVT4 promoter. Previous microarray results were confirmed that gln3∆gat1∆ cells showed a decrease in expression of AVT1 and AVT7, which also encode vacuolar amino acid transporters. Additionally, ChIP analysis revealed that the AVT6 encoding vacuolar acidic amino acid exporter represents a new direct target of the GATA transcription factor. The broad effect of the GATA transcription factors on the expression of AVT transporters suggests that vacuolar amino acid transport is integrated into cellular amino acid homeostasis.

Genetic control of dorsal-ventral identity in the telencephalon: opposing roles for Pax6 and Gsh2

Development ◽  
2000 ◽  
Vol 127 (20) ◽  
pp. 4361-4371 ◽  
Author(s):  
H. Toresson ◽  
S.S. Potter ◽  
K. Campbell
Keyword(s):  
Cerebral Cortex ◽  
Gene Function ◽  
Abnormal Development ◽  
Loss Of Function ◽  
Embryonic Mouse ◽  
Molecular Identity ◽  
Mouse Mutants ◽  
Germinal Zone ◽  
Genetic Mechanisms ◽  
Dlx Genes

We have examined the genetic mechanisms that regulate dorsal-ventral identity in the embryonic mouse telencephalon and, in particular, the specification of progenitors in the cerebral cortex and striatum. The respective roles of Pax6 and Gsh2 in cortical and striatal development were studied in single and double loss-of-function mouse mutants. Gsh2 gene function was found to be essential to maintain the molecular identity of early striatal progenitors and in its absence the ventral telencephalic regulatory genes Mash1 and Dlx are lost from most of the striatal germinal zone. In their place, the dorsal regulators, Pax6, neurogenin 1 and neurogenin 2 are found ectopically. Conversely, Pax6 is required to maintain the correct molecular identity of cortical progenitors. In its absence, neurogenins are lost from the cortical germinal zone and Gsh2, Mash1 and Dlx genes are found ectopically. These reciprocal alterations in cortical and striatal progenitor specification lead to the abnormal development of the cortex and striatum observed in Pax6 (small eye) and Gsh2 mutants, respectively. In support of this, double homozygous mutants for Pax6 and Gsh2 exhibit significant improvements in both cortical and striatal development compared with their respective single mutants. Taken together, these results demonstrate that Pax6 and Gsh2 govern cortical and striatal development by regulating genetically opposing programs that control the expression of each other as well as the regionally expressed developmental regulators Mash1, the neurogenins and Dlx genes in telencephalic progenitors.

The Drosophila dCREB-A gene is required for dorsal/ventral patterning of the larval cuticle

Development ◽  
1997 ◽  
Vol 124 (1) ◽  
pp. 181-193 ◽  
Author(s):  
D.J. Andrew ◽  
A. Baig ◽  
P. Bhanot ◽  
S.M. Smolik ◽  
K.D. Henderson
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Signaling Cascades ◽  
Loss Of Function ◽  
Larval Cuticle ◽  
Extracellular Signals ◽  
Patterning Genes ◽  
Lateral Structures ◽  
Cuticular Structures

We report on the characterization of the first loss-of-function mutation in a Drosophila CREB gene, dCREB-A. In the epidermis, dCREB-A is required for patterning cuticular structures on both dorsal and ventral surfaces since dCREB-A mutant larvae have only lateral structures around the entire circumference of each segment. Based on results from epistasis tests with known dorsal/ventral patterning genes, we propose that dCREB-A encodes a transcription factor that functions near the end of both the DPP- and SPI-signaling cascades to translate the corresponding extracellular signals into changes in gene expression. The lateralizing phenotype of dCREB-A mutants reveals a much broader function for CREB proteins than previously thought.

scholarly journals Identification of MEF2-regulated genes during muscle differentiation

2004 ◽  
Vol 20 (1) ◽  
pp. 143-151 ◽  
Author(s):  
James Paris ◽  
Carl Virtanen ◽  
Zhibin Lu ◽  
Mark Takahashi
Keyword(s):  
Gene Regulation ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Neuromuscular Junctions ◽  
Muscle Differentiation ◽  
Signaling Cascades ◽  
Specific Gene ◽  
Genetic Mechanisms ◽  
Selection Parameters ◽  
First Time

Although a great deal has been elucidated concerning the mechanisms regulating muscle differentiation, little is known about transcription factor-specific gene regulation. Our understanding of the genetic mechanisms regulating cell differentiation is quite limited. Much of what has been defined centers on regulatory signaling cascades and transcription factors. Surprisingly few studies have investigated the association of genes with specific transcription factors. To address these issues, we have utilized a method coupling chromatin immunoprecipitation and CpG microarrays to characterize the genes associated with MEF2 in differentiating C2C12 cells. Results demonstrated a defined binding pattern over the course of differentiation. Filtered data demonstrated 9 clones to be elevated at 0 h, 792 at 6 h, 163 by 1 day, and 316 at 3 days. Using unbiased selection parameters, we selected a subset of 291 prospective candidates. Clones were sequenced and filtered for removal of redundancy between clones and for the presence of repetitive elements. We were able to place 50 of these on the mouse genome, and 20 were found to be located near well-annotated genes. From this list, previously undefined associations with MEF2 were discovered. Many of these genes represent proteins involved in neurogenesis, neuromuscular junctions, signaling and metabolism. The remaining clones include many full-length cDNA and represent novel gene targets. The results of this study provides for the first time, a unique look at gene regulation at the level of transcription factor binding in differentiating muscle.

Sign in / Sign up

Export Citation Format

Share Document