scholarly journals Molecular basis of fatty acid taste in Drosophila

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Ji-Eun Ahn ◽  
Yan Chen ◽  
Hubert Amrein
Keyword(s):  
Fatty Acids ◽  
Behavioral Responses ◽  
Hexanoic Acid ◽  
Wild Type ◽  
Cell Type ◽  
Ionotropic Receptor ◽  
Behavioral Studies ◽  
Cell Type Specific ◽  
Receptor Neurons ◽  
Ir Genes

Behavioral studies have established that Drosophila appetitive taste responses towards fatty acids are mediated by sweet sensing Gustatory Receptor Neurons (GRNs). Here we show that sweet GRN activation requires the function of the Ionotropic Receptor genes IR25a, IR76b and IR56d. The former two IR genes are expressed in several neurons per sensillum, while IR56d expression is restricted to sweet GRNs. Importantly, loss of appetitive behavioral responses to fatty acids in IR25a and IR76b mutant flies can be completely rescued by expression of respective transgenes in sweet GRNs. Interestingly, appetitive behavioral responses of wild type flies to hexanoic acid reach a plateau at ~1%, but decrease with higher concentration, a property mediated through IR25a/IR76b independent activation of bitter GRNs. With our previous report on sour taste, our studies suggest that IR-based receptors mediate different taste qualities through cell-type specific IR subunits.

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

scholarly journals Molecular and cellular adaptations in hippocampal parvalbumin neurons mediate behavioral responses to chronic social stress

2021 ◽  
Author(s):  
Dionnet L Bhatti ◽  
Lucian Medrihan ◽  
Michelle X Chen ◽  
Junghee Jin ◽  
Kathryn McCabe ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Affinity Purification ◽  
Behavioral Outcomes ◽  
Behavioral Responses ◽  
Specific Gene ◽  
Mrna Levels ◽  
Cell Type ◽  
Stress Resilience ◽  
Cell Type Specific ◽  
Stress Susceptibility

BACKGROUND: Behavioral responses to stress are, in part, mediated by the hippocampus and Parvalbumin (PV)-expressing neurons. However, whether chronic stress induces molecular and cellular adaptations in hippocampal PV neurons contribute to stress-induced behavioral outcomes remains elusive. METHOD: Using chronic social defeat stress (CSDS), we investigated the role of neuronal activity and gene expression in hippocampal PV neurons in mediating stress-resilience and -susceptibility. We first used in vivo high-density silicon probe recordings and chemogenetics to test whether the activity of PV neurons in ventral dentate gyrus (PVvDG) is associated with particular behavioral outcomes. To find critical molecular pathways associated with stress-resilience and -susceptibility, we used PV-neuron-selective translating ribosome affinity purification and RNAseq. We used immunoblotting, RNAscope, and region- or cell type-specific gene deletion to determine whether Ahnak, a molecule regulating depression-like behavior, was necessary for behavioral divergence after CSDS. RESULTS: We find CSDS modulates neuronal activity in vDG. Notably, stress-susceptibility is associated with an increase of PVvDG firing, which we find is necessary and sufficient for susceptibility. Additionally, genes involved in mitochondrial function, protein synthesis and synaptogenesis are differentially expressed in hippocampal PV neurons of stress-resilient and -susceptible mice. Interestingly, protein and mRNA levels of Ahnak, an endogenous regulator of L-type calcium channels are associated with susceptibility after CSDS. vDG- and PV cell type-specific deletions reveal that Ahnak is required for stress-susceptibility to CSDS. CONCLUSIONS: These findings indicate that CSDS-induced molecular and cellular adaptations in hippocampal PV neurons mediate behavioral consequences, proposing a mechanism underlying individual differences in stress vulnerability.

scholarly journals Complementation between mouse Mfn1 and Mfn2 protects mitochondrial fusion defects caused by CMT2A disease mutations

2007 ◽  
Vol 176 (4) ◽  
pp. 405-414 ◽  
Author(s):  
Scott A. Detmer ◽  
David C. Chan
Keyword(s):  
Axonal Degeneration ◽  
Mitochondrial Protein ◽  
Mitochondrial Fusion ◽  
Wild Type ◽  
Cell Type ◽  
Charcot Marie Tooth Disease ◽  
Disease Mutations ◽  
Cell Type Specific ◽  
In Trans ◽  
Tooth Disease

Mfn2, an oligomeric mitochondrial protein important for mitochondrial fusion, is mutated in Charcot-Marie-Tooth disease (CMT) type 2A, a peripheral neuropathy characterized by axonal degeneration. In addition to homooligomeric complexes, Mfn2 also associates with Mfn1, but the functional significance of such heterooligomeric complexes is unknown. Also unknown is why Mfn2 mutations in CMT2A lead to cell type–specific defects given the widespread expression of Mfn2. In this study, we show that homooligomeric complexes formed by many Mfn2 disease mutants are nonfunctional for mitochondrial fusion. However, wild-type Mfn1 complements mutant Mfn2 through the formation of heterooligomeric complexes, including complexes that form in trans between mitochondria. Wild-type Mfn2 cannot complement the disease alleles. Our results highlight the functional importance of Mfn1–Mfn2 heterooligomeric complexes and the close interplay between the two mitofusins in the control of mitochondrial fusion. Furthermore, they suggest that tissues with low Mfn1 expression are vulnerable in CMT2A and that methods to increase Mfn1 expression in the peripheral nervous system would benefit CMT2A patients.

scholarly journals Control of Cell Type Proportioning in Dictyostelium discoideum by Differentiation-Inducing Factor as Determined by In Situ Hybridization

2004 ◽  
Vol 3 (5) ◽  
pp. 1241-1248 ◽  
Author(s):  
Toshinari Maruo ◽  
Haruyo Sakamoto ◽  
Negin Iranfar ◽  
Danny Fuller ◽  
Takahiro Morio ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Dictyostelium Discoideum ◽  
Wild Type ◽  
Cell Type ◽  
Type Conversion ◽  
New Genes ◽  
A Cell ◽  
Cell Type Specific ◽  
Cell Type Conversion

ABSTRACT We have determined the proportions of the prespore and prestalk regions in Dictyostelium discoideum slugs by in situ hybridization with a large number of prespore- and prestalk-specific genes. Microarrays were used to discover genes expressed in a cell type-specific manner. Fifty-four prespore-specific genes were verified by in situ hybridization, including 18 that had been previously shown to be cell type specific. The 36 new genes more than doubles the number of available prespore markers. At the slug stage, the prespore genes hybridized to cells uniformly in the posterior 80% of wild-type slugs but hybridized to the posterior 90% of slugs lacking the secreted alkylphenone differentiation-inducing factor 1 (DIF-1). There was a compensatory twofold decrease in prestalk cells in DIF-less slugs. Removal of prespore cells resulted in cell type conversion in both wild-type and DIF-less anterior fragments. Thus, DIF-1 appears to act in concert with other processes to establish cell type proportions.

scholarly journals Integrins Have Cell-Type-Specific Roles in the Development of Motor Neuron Connectivity

2019 ◽  
Vol 7 (3) ◽  
pp. 17 ◽  
Author(s):  
Devyn Oliver ◽  
Emily Norman ◽  
Heather Bates ◽  
Rachel Avard ◽  
Monika Rettler ◽  
...  
Keyword(s):  
Nervous System ◽  
Cell Adhesion ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Neuron Development ◽  
Wild Type ◽  
Cell Type ◽  
C Elegans ◽  
Cell Type Specific ◽  
Two Phases

Formation of the nervous system requires a complex series of events including proper extension and guidance of neuronal axons and dendrites. Here we investigate the requirement for integrins, a class of transmembrane cell adhesion receptors, in regulating these processes across classes of C. elegans motor neurons. We show α integrin/ina-1 is expressed by both GABAergic and cholinergic motor neurons. Despite this, our analysis of hypomorphic ina-1(gm144) mutants indicates preferential involvement of α integrin/ina-1 in GABAergic commissural development, without obvious involvement in cholinergic commissural development. The defects in GABAergic commissures of ina-1(gm144) mutants included both premature termination and guidance errors and were reversed by expression of wild type ina-1 under control of the native ina-1 promoter. Our results also show that α integrin/ina-1 is important for proper outgrowth and guidance of commissures from both embryonic and post-embryonic born GABAergic motor neurons, indicating an ongoing requirement for integrin through two phases of GABAergic neuron development. Our findings provide insights into neuron-specific roles for integrin that would not be predicted based solely upon expression analysis.

Cell-type-specific rescue of myosin function during Dictyostelium development defines two distinct cell movements required for culmination

Development ◽  
1998 ◽  
Vol 125 (19) ◽  
pp. 3895-3903 ◽  
Author(s):  
T.L. Chen ◽  
W.A. Wolf ◽  
R.L. Chisholm
Keyword(s):  
Fluorescent Protein ◽  
Video Recording ◽  
Time Lapse ◽  
Active Movement ◽  
Upward Movement ◽  
Wild Type ◽  
Cell Type ◽  
Developmental Defects ◽  
Distinct Cell ◽  
Cell Type Specific

Mutant Dictyostelium cells lacking any of the component polypeptides of myosin II exhibit developmental defects. To define myosin's role in establishing Dictyostelium's developmental pattern, we have rescued myosin function in a myosin regulatory light chain null mutant (mlcR-) using cell-type-specific promoters. While mlcR- cells fail to progress beyond the mound stage, expression of RLC from the prestalk promoter, ecmA, produces culminants with normal stalks but with defects in spore cell localization. When GFP-marked prestalk and prespore cells expressing ecmA-RLC are mixed with wild-type cells, the mislocalization of prestalk cells, but not prespore cells, is rescued. Time-lapse video recording of ecmA-RLC cells showed that the posterior prespore zone failed to undergo a contraction important for the upward movement of prespore cells. Prespore cells marked with green fluorescent protein (GFP) failed to move toward the tip with the spiral motion typical of wild type. In contrast, expression of RLC in prespore cells using the psA promoter produced balloon-like structures reminiscent of sorocarps but lacking stalks. GFP-labeled prespore cells showed a spiral movement toward the top of the structures. Expression of RLC from the psA promoter restores the normal localization of psA-GFP cells, but not ecmA-GFP cells. These results define two distinct, myosin-dependent movements that are required for establishing a Dictyostelium fruiting body: stalk extension and active movement of the prespore zone that ensures proper placement of the spores atop the stalk. The approach used in these studies provides a direct means of testing the role of cell motility in distinct cell types during a morphogenetic program.

scholarly journals A Ubiquitin-Conjugating Enzyme Is Essential for Developmental Transitions in Dictyostelium

1997 ◽  
Vol 8 (10) ◽  
pp. 1989-2002 ◽  
Author(s):  
Alexandra Clark ◽  
Anson Nomura ◽  
Sudhasri Mohanty ◽  
Richard A. Firtel
Keyword(s):  
Gene Expression ◽  
Amino Acid ◽  
Amino Acid Sequence ◽  
Specific Gene ◽  
Wild Type ◽  
Cell Type ◽  
Protein Ubiquitination ◽  
High Amino Acid ◽  
Cell Type Specific ◽  
Very High

We have identified a developmentally essential gene,UbcB, by insertional mutagenesis. The encoded protein (UBC1) shows very high amino acid sequence identity to ubiquitin-conjugating enzymes from other organisms, suggesting that UBC1 is involved in protein ubiquitination and possibly degradation during Dictyostelium development. Consistent with the homology of the UBC1 protein to UBCs, the developmental pattern of protein ubiquitination is altered in ubcB-null cells.ubcB-null cells are blocked in the ability to properly execute the developmental transition that occurs between the induction of postaggregative gene expression during mound formation and the induction of cell-type differentiation and subsequent morphogenesis.ubcB-null cells plated on agar form mounds with normal kinetics; however, they remain at this stage for ∼10 h before forming multiple tips and fingers that then arrest. Under other conditions, some of the fingers form migrating slugs, but no culmination is observed. In ubcB-null cells, postaggregative gene transcripts accumulate to very high levels and do not decrease significantly with time as they do in wild-type cells. Expression of cell-type-specific genes is very delayed, with the level of prespore-specific gene expression being significantly reduced compared with that in wild-type cells. lacZ reporter studies using developmentally regulated and cell-type-specific promoters suggest that ubcB-null cells show an unusually elevated level of staining of lacZ reporters expressed in anterior-like cells, a regulatory cell population found scattered throughout the aggregate, and reduced staining of a prespore reporter.ubcB-null cells in a chimeric organism containing predominantly wild-type cells are able to undergo terminal differentiation but show altered spatial localization. In contrast, in chimeras containing only a small fraction of wild-type cells, the mature fruiting body is very small and composed almost exclusively of wild-type cells, with the ubcB-null cells being present as a mass of cells located in extreme posterior of the developing organism. The amino acid sequence analysis of the UbcBopen reading frame (ORF) and the analysis of the developmental phenotypes suggest that tip formation and subsequent development requires specific protein ubiquitination, and possibly degradation.

scholarly journals Repeated Passage of Wild-Type Woodchuck Hepatitis Virus in Lymphoid Cells Does Not Generate Cell Type-Specific Variants or Alter Virus Infectivity

2008 ◽  
Vol 82 (15) ◽  
pp. 7540-7550 ◽  
Author(s):  
Patricia M. Mulrooney-Cousins ◽  
Tomasz I. Michalak
Keyword(s):  
Lymphatic System ◽  
Hepatitis Virus ◽  
Cell Types ◽  
Lymphoid Cells ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Cell Type ◽  
Cell Type Specific ◽  
Repeated Passage

ABSTRACT Woodchuck hepatitis virus (WHV), which is closely related to human hepatitis B virus, infects the liver but also invariably establishes persistent infection in the lymphatic system. Although the dose of invading virus appears to be the main factor in determining whether WHV infection is restricted to the lymphatic system or also engages the liver, the nature of WHV lymphotropism remains unclear and a role for a specific lymphotropic variant was not excluded. The availability of woodchuck lymphocyte and hepatocyte cultures susceptible to WHV infection allows investigation of this issue in vitro. We hypothesized that repeated passage of wild-type WHV in lymphoid cells should lead to enrichment of a lymphotropic virus variant, if in fact such a variant exists. For this purpose, wild-type WHV with a homogeneous sequence was used as the inoculum, while lymphoid cells from a single healthy woodchuck donor and a normal woodchuck WCM-260 hepatocyte line served as infection targets. The serial passage of the wild-type virus repeated up to 13 times for both cell types did not lead to the emergence of cell type-specific WHV variants, as revealed by sequence analysis of the virus envelope and the core and X gene sequences. Moreover, the virus passaged in both cell types remained infectious for naive woodchucks, produced infection profiles that depended upon virus dose but not on virus cellular origin, and retained its initial DNA sequence. These results imply that WHV lymphotropism is a natural propensity of the wild-type virus and is not a consequence of infection with a viral variant.

scholarly journals Jasmonate biosynthesis arising from altered cell walls is prompted by turgor-driven mechanical compression

2021 ◽  
Vol 7 (7) ◽  
pp. eabf0356
Author(s):  
Stefan Mielke ◽  
Marlene Zimmer ◽  
Mukesh Kumar Meena ◽  
René Dreos ◽  
Hagen Stellmach ◽  
...  
Keyword(s):  
Cell Walls ◽  
Turgor Pressure ◽  
Mechanical Compression ◽  
Wild Type ◽  
Cell Type ◽  
Cortex Cell ◽  
Seedling Roots ◽  
Cell Type Specific ◽  
Altered Cell

Despite the vital roles of jasmonoyl-isoleucine (JA-Ile) in governing plant growth and environmental acclimation, it remains unclear what intracellular processes lead to its induction. Here, we provide compelling genetic evidence that mechanical and osmotic regulation of turgor pressure represents a key elicitor of JA-Ile biosynthesis. After identifying cell wall mutant alleles in KORRIGAN1 (KOR1) with elevated JA-Ile in seedling roots, we found that ectopic JA-Ile resulted from cell nonautonomous signals deriving from enlarged cortex cells compressing inner tissues and stimulating JA-Ile production. Restoring cortex cell size by cell type–specific KOR1 complementation, by isolating a genetic kor1 suppressor, and by lowering turgor pressure with hyperosmotic treatments abolished JA-Ile signaling. Conversely, hypoosmotic treatment activated JA-Ile signaling in wild-type plants. Furthermore, constitutive JA-Ile levels guided mutant roots toward greater water availability. Collectively, these findings enhance our understanding on JA-Ile biosynthesis initiation and reveal a previously undescribed role of JA-Ile in orchestrating environmental resilience.

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