scholarly journals INDEHISCENT regulates explosive seed dispersal

2021 ◽  
Author(s):  
Anahit Galstyan ◽  
Penny Sarchet ◽  
Rafael Campos-Martin ◽  
Milad Adibi ◽  
Lachezar A Nikolov ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Types ◽  
Negative Regulator ◽  
Bhlh Transcription Factor ◽  
Zone Formation ◽  
Distinct Cell ◽  
Developmental System Drift ◽  
Dehiscence Zone ◽  
Conserved Gene ◽  
Open Question

How traits evolve to produce novelty or stasis is an open question in biology. We investigate this question in Cardamine hirsuta, a relative of Arabidopsis thaliana that employs explosive fracture to disperse its seeds. This trait evolved through key morphomechanical innovations that distinguish the otherwise very similar, dehiscent fruit of these two species. Using CRISPR/Cas9, we show that dehiscence zone formation is absolutely required for explosive fracture in C. hirsuta, and is controlled by the bHLH transcription factor INDEHISCENT (IND). Using mutant screens, we identified the MADS-box transcription factor FRUITFULL (FUL) as a negative regulator of IND in C. hirsuta. Although FUL function is conserved in C. hirsuta, the consequences of IND mis-expression differ in ful mutants of C. hirsuta versus A. thaliana. In ful mutants of both species, valve tissue is replaced by dehiscence zone tissue, which comprises two distinct cell types: lignified layer and separation layer cells. While A. thaliana ful mutants develop stunted fruit with ectopic lignified layer cells, C. hirsuta ful mutants have elongated fruit with ectopic separation layer cells. We show that IND dose determines the proportion of these two cell types in ectopic dehiscence zones. We also show that the extent of ectopic lignification caused by IND mis-expression determines fruit length. Our findings indicate developmental system drift in the conserved gene network patterning dehiscent fruit in two related Brassicaceae species.

scholarly journals p19ARF Is Dispensable for Oncogenic Stress-Induced p53-Mediated Apoptosis and Tumor Suppression In Vivo

2002 ◽  
Vol 22 (1) ◽  
pp. 370-377 ◽  
Author(s):  
Dawn Tolbert ◽  
Xiangdong Lu ◽  
Chaoying Yin ◽  
Mathew Tantama ◽  
Terry Van Dyke
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppression ◽  
Tumor Model ◽  
Cell Types ◽  
Negative Regulator ◽  
Suppressor Activity ◽  
Distinct Cell ◽  
Tumor Suppressor Activity ◽  
Oncogenic Stress

ABSTRACT Recent studies have shown the p19ARF tumor suppressor to be involved in the response to oncogenic stress by regulating the activity of p53. This response is mediated by antagonizing the function of Mdm2, a negative regulator of p53, indicating a pathway for tumor suppression that involves numerous genes altered in human tumors. We previously described a transgenic mouse brain tumor model in which oncogenic stress, provided by cell-specific inactivation of the pRb pathway, triggers a p53-dependent apoptotic response. This response suppresses the growth of developing tumors and thus represents a bona fide in vivo tumor suppressor activity. We further showed that E2F1, a transcription factor known to induce p19ARF expression, was required for the response. Here, we use a genetic approach to test whether p19ARF functions to transduce the signal from E2F1 to p53 in this tumor suppression pathway. Contrary to the currently accepted hypothesis, we show that a deficiency in p19ARF has no impact on p53-mediated apoptosis or tumor suppression in this system. All measures of p53 function, including the level of apoptosis induced by pRb inactivation, the expression of p21 (a p53-responsive gene), and the rate of tumor growth, were comparable in mice with and without a functional p19ARF gene. Thus, although p19ARF is required in some cell types to transmit an oncogenic response signal to p53, it is dispensable for this function in an in vivo epithelial system. These results underscore the complexity of p53 tumor suppression and further indicate the existence of distinct cell-specific pathways that respond to similar stimuli.

scholarly journals Loss of function of bHLH transcription factor Nrd1 in tomato induces an arabinogalactan protein-encoding gene and enhances resistance to Pseudomonas syringae pv. tomato

2021 ◽  
Author(s):  
Ning Zhang ◽  
Chloe Hecht ◽  
Xuepeng Sun ◽  
Zhangjun Fei ◽  
Gregory B Martin
Keyword(s):  
Transcription Factor ◽  
Pseudomonas Syringae ◽  
Transcript Abundance ◽  
Negative Regulator ◽  
Arabinogalactan Protein ◽  
Bhlh Transcription Factor ◽  
Dependent Manner ◽  
Rna Seq ◽  
Loss Of Function ◽  
Encoding Gene

Basic helix-loop-helix (bHLH) transcription factors constitute a superfamily in eukaryotes but their roles in plant immunity remain largely uncharacterized. We found that the transcript abundance in tomato leaves of one bHLH transcription factor-encoding gene, Nrd1 (negative regulator of resistance to DC3000 1), was significantly increased after treatment with the immunity-inducing flgII-28 peptide. Plants carrying a loss-of-function mutation in Nrd1 (Δnrd1) showed enhanced resistance to Pseudomonas syringae pv. tomato (Pst) DC3000 although early pattern-triggered immunity responses such as generation of reactive oxygen species and activation of mitogen-activated protein kinases after treatment with flagellin-derived flg22 and flgII-28 peptides were unaltered compared to wild-type plants. An RNA-Seq analysis identified a gene, Agp1, whose expression is strongly suppressed in an Nrd1-dependent manner. Agp1 encodes an arabinogalactan protein and overexpression of the Agp1 gene in Nicotiana benthamiana led to ~10-fold less Pst growth compared to the control. These results suggest that the Nrd1 protein promotes tomato susceptibility to Pst by suppressing the defense gene Agp1. RNA-Seq also revealed that loss of Nrd1 function has no effect on the transcript abundance of immunity-associated genes including Bti9, Core, Fls2, Fls3 and Wak1 upon Pst inoculation, suggesting that the enhanced immunity observed in the Δnrd1 mutants is due to the activation of key PRR signaling components as well as loss of Nrd1-regulated suppression of Agp1.

The basic-helix-loop-helix protein pod1 is critically important for kidney and lung organogenesis

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5771-5783 ◽  
Author(s):  
S.E. Quaggin ◽  
L. Schwartz ◽  
S. Cui ◽  
P. Igarashi ◽  
J. Deimling ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Perinatal Period ◽  
Branching Morphogenesis ◽  
Bhlh Transcription Factor ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Kidney Morphogenesis

Epithelial-mesenchymal interactions are required for the development of all solid organs but few molecular mechanisms that underlie these interactions have been identified. Pod1 is a basic-helix-loop-helix (bHLH) transcription factor that is highly expressed in the mesenchyme of developing organs that include the lung, kidney, gut and heart and in glomerular visceral epithelial cells (podocytes). To determine the function of Pod1 in vivo, we have generated a lacZ-expressing null Pod1 allele. Null mutant mice are born but die in the perinatal period with severely hypoplastic lungs and kidneys that lack alveoli and mature glomeruli. Although Pod1 is exclusively expressed in the mesenchyme and podocytes, major defects are observed in the adjacent epithelia and include abnormalities in epithelial differentiation and branching morphogenesis. Pod1 therefore appears to be essential for regulating properties of the mesenchyme that are critically important for lung and kidney morphogenesis. Defects specific to later specialized cell types where Pod1 is expressed, such as the podocytes, were also observed, suggesting that this transcription factor may play multiple roles in kidney morphogenesis.

scholarly journals BETA3, a novel helix-loop-helix protein, can act as a negative regulator of BETA2 and MyoD-responsive genes.

1996 ◽  
Vol 16 (2) ◽  
pp. 626-633 ◽  
Author(s):  
M Peyton ◽  
C M Stellrecht ◽  
F J Naya ◽  
H P Huang ◽  
P J Samora ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Negative Regulator ◽  
Bhlh Transcription Factor ◽  
Pcr Cloning ◽  
Specific Expression ◽  
Class A ◽  
Helix Loop Helix ◽  
E Box ◽  
Class B ◽  
Bhlh Factors

Using degenerate PCR cloning we have identified a novel basic helix-loop-helix (bHLH) transcription factor, BETA3, from a hamster insulin tumor (HIT) cell cDNA library. Sequence analysis revealed that this factor belongs to the class B bHLH family and has the highest degree of homology with another bHLH transcription factor recently isolated in our laboratory, BETA2 (neuroD) (J. E. Lee, S. M. Hollenberg, L. Snider, D. L. Turner, N. Lipnick, and H. Weintraub, Science 268:836-844, 1995; F. J. Naya, C. M. M. Stellrecht, and M.-J. Tsai, Genes Dev. 8:1009-1019, 1995). BETA2 is a brain- and pancreatic-islet-specific bHLH transcription factor and is largely responsible for the tissue-specific expression of the insulin gene. BETA3 was found to be tissue restricted, with the highest levels of expression in HIT, lung, kidney, and brain cells. Surprisingly, despite the homology between BETA2 and BETA3 and its intact basic region, BETA3 is unable to bind the insulin E box in bandshift analysis as a homodimer or as a heterodimer with the class A bHLH factors E12, E47, or BETA1. Instead, BETA3 inhibited both the E47 homodimer and the E47/BETA2 heterodimer binding to the insulin E box. In addition, BETA3 greatly repressed the BETA2/E47 induction of the insulin enhancer in HIT cells as well as the MyoD/E47 induction of a muscle-specific E box in the myoblast cell line C2C12. In contrast, expression of BETA3 had no significant effect on the GAL4-VP16 transcriptional activity. Immunoprecipitation analysis demonstrates that the mechanism of repression is via direct protein-protein interaction, presumably by heterodimerization between BETA3 and class A bHLH factors.

scholarly journals Cell-intrinsic functions of the transcription factor Bhlhe40 in activated B cells and T follicular helper cells restrain the germinal center reaction and prevent lymphomagenesis

2021 ◽  
Author(s):  
René Rauschmeier ◽  
Annika Reinhardt ◽  
Charlotte Gustafsson ◽  
Vassilis Glaros ◽  
Artem V. Artemov ◽  
...  
Keyword(s):  
Transcription Factor ◽  
B Cells ◽  
Germinal Center ◽  
B Cell Lymphoma ◽  
Cell Types ◽  
Negative Regulator ◽  
Germinal Center Reaction ◽  
Follicular Helper ◽  
Positive Regulators ◽  
Early Memory

ABSTRACTThe generation of high-affinity antibodies against pathogens and vaccines requires the germinal center (GC) reaction – a process that relies on a complex interplay between specialized effector subsets of B and CD4 T lymphocytes – GC B cells and T follicular helper (TFH) cells. Intriguingly, several key positive regulators of the GC reaction are common for both cell types. Here, we report that the transcription factor Bhlhe40 is a crucial cell-intrinsic negative regulator affecting both the B and T cell sides of the GC reaction. In activated CD4 T cells, Bhlhe40 was required to restrain proliferation thus limiting the number of TFH cells. In B cells, Bhlhe40 executed its function in the first days after immunization by selectively restricting the generation of the earliest GC B cells but not of early memory B cells or plasmablasts. Conditional Bhlhe40 inactivation confirmed cell-autonomous functions of Bhlhe40 in both GC B and TFH cells, while the GC phenotype was further enhanced upon loss of Bhlhe40 in both cell types. This negative regulation of the GC reaction by Bhlhe40 was of crucial importance, as Bhlhe40-deficient mice with progressing age succumbed to a B cell lymphoma characterized by accumulation of monoclonal GC B-like cells and polyclonal TFH cells in various tissues.

Fine Structure of the Malpighian Tubules of the Mosquito, Culex pipiens

1971 ◽  
Vol 29 ◽  
pp. 402-403
Author(s):  
Brendan Clifford
Keyword(s):  
Fine Structure ◽  
Culex Pipiens ◽  
Stellate Cell ◽  
Malpighian Tubule ◽  
Cell Types ◽  
Instar Larva ◽  
Malpighian Tubules ◽  
Calliphora Erythrocephala ◽  
Distinct Cell ◽  
Basal Plasma

An ultrastructural investigation of the Malpighian tubules of the fourth instar larva of Culex pipiens was undertaken as part of a continuing study of the fine structure of transport epithelia.Each of the five Malpighian tubules was found to be morphologically identical and regionally undifferentiated. Two distinct cell types, the primary and stellate, were found intermingled along the length of each tubule. The ultrastructure of the stellate cell was previously described in the Malpighian tubule of the blowfly, Calliphora erythrocephala by Berridge and Oschman.The basal plasma membrane of the primary cell is extremely irregular, giving rise to a complex interconnecting network of basal channels. The compartments of cytoplasm entrapped within this system of basal infoldings contain mitochondria, free ribosomes, and small amounts of rough endoplasmic reticulum. The mitochondria are distinctive in that the cristae run parallel to the long axis of the organelle.

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