Fine structure of the antennal sensory appendix in the larva of Ctenicera destructor (Brown) (Elateridae: Coleoptera)

1971 ◽  
Vol 49 (2) ◽  
pp. 199-210 ◽  
Author(s):  
David A. Scott ◽  
R. Y. Zacharuk
Keyword(s):  
Sense Organ ◽  
Proximal Region ◽  
Central Complex ◽  
Body Region ◽  
Type I ◽  
Fiber System ◽  
Dendritic Branches ◽  
Membranous Septum ◽  
Complex Junction ◽  
Ctenicera Destructor

The antennal sensory appendix of Ctenicera destructor (Brown) appears to be a compound sensillum basiconicum formed by a union of about 12 individual sensilla. It is innervated by about 36 bipolar sense cells of type I, which occur usually in 12 groups of three neurons each. The sensory cuticle is large, cone-shaped, and abundantly perforated by a slit-tubule system. The dendrites of each group of neurons are enclosed distally by a single tubular cuticular sheath attached to the base of the cone by a suspensory fiber system. The ensheathed portion of the dendrites lies in a receptor-lymph cavity formed by the tormogen and accessory trophic cells. Distal dendritic branches pass below and occasionally enter inner pockets in the sensory cuticle, but no connections were seen between the slit-tubule system and the dendritic surfaces. About 12 of each of four types of cells are associated with the neurons in this sensillum: tormogen, trichogen, accessory trophic, and neurilemma. The ultrastructure and probable function of each type is described. A central, complex junction body region divides each dendrite into morphologically distinct distal and proximal region. All the cells associated with the sensillum are in a compact bundle, which is separated from adjacent sensilla within the antenna by a membranous septum. It is suggested that this sense organ has an olfactory function.

Fine structure of the dendritic junction body region of the antennal sensory cone in a larval elaterid (Coleoptera)

1971 ◽  
Vol 49 (6) ◽  
pp. 817-821 ◽  
Author(s):  
David A. Scott ◽  
R. Y. Zacharuk
Keyword(s):  
Fine Structure ◽  
Basal Body ◽  
Sense Organ ◽  
Body Region ◽  
Ultrastructural Evidence ◽  
Primary Function ◽  
Secretory Products

The component ciliary collar, basal body, ciliary rootlets, trichogen–dendrite secretory junctions and secretory inclusions of the junction body region of dendrites in the wireworm antennal sensory cone are described. The primary function ascribed to the junction body region, based on the ultrastructural evidence presented, is one of secretion. The hypothesis that the secretory products produced in the junction body region are transported to the dendritic terminations in the sense organ is discussed and supported.

scholarly journals Histological and histochemical aspects of the penial glands of Girardia biapertura Sluys, 1997 (Platyhelminthes, Tricladida, Paludicola)

2002 ◽  
Vol 62 (3) ◽  
pp. 547-555 ◽  
Author(s):  
S. T. SOUZA ◽  
A. M. LEAL-ZANCHET
Keyword(s):  
Secretory Cell ◽  
Ejaculatory Duct ◽  
Distal Portion ◽  
Proximal Region ◽  
Secretory Cells ◽  
Type I ◽  
Type Ii ◽  
Cell Type ◽  
Median Region

Girardia biapertura was described with sperm ducts penetrating the penis bulb, subsequently opening separately at the tip of the penis papilla and receiving the abundant secretion of penial glands. In the present work, the penial glands of this species have been histologically and histochemically analysed, and four types of secretory cells are distinguished. The openings of the penial glands into the intrabulbar and intrapapillar sperm ducts, designated here as intrapenial ducts, allow for the distinction between three histologically differentiated regions. The most proximal region possibly corresponds to the bulbar cavity of other freshwater triclads whereas the median and distal portions correspond to the ejaculatory duct. The proximal region of the intrapenial ducts receives mainly the openings of a secretory cell type (type I) that produces a proteinaceous secretion. A second type of secretory cell (type II) that secretes neutral mucopolyssacharides opens into the median region of the intrapenial ducts. The distal portion of the ducts receives two types of secretory cells (types III and IV) which secret glycoprotein and glycosaminoglycans, respectively. Types III and IV open also directly into the male atrium through the epithelium of the penis papilla. A comparison with the results presented here and those of other authors for species of Girardia is provided and the importance of the study of the penial glands for taxonomic characterisation of freshwater triclads is emphasised.

scholarly journals Genetic basis of the formation and identity of type I and type II neurons in Drosophila embryos

Development ◽  
1997 ◽  
Vol 124 (14) ◽  
pp. 2819-2828 ◽  
Author(s):  
M. Vervoort ◽  
D.J. Merritt ◽  
A. Ghysen ◽  
C. Dambly-Chaudiere
Keyword(s):  
Cell Communication ◽  
Sense Organ ◽  
Type I ◽  
Type Ii ◽  
Neuronal Fate ◽  
Late Step ◽  
Alternative Type ◽  
The Difference ◽  
Dependent Lineages ◽  
Multidendritic Neurons

The embryonic peripheral nervous system of Drosophila contains two main types of sensory neurons: type I neurons, which innervate external sense organs and chordotonal organs, and type II multidendritic neurons. Here, we analyse the origin of the difference between type I and type II in the case of the neurons that depend on the proneural genes of the achaete-scute complex (ASC). We show that, in Notch- embryos, the type I neurons are missing while type II neurons are produced in excess, indicating that the type I/type II choice relies on Notch-mediated cell communication. In contrast, both type I and type II neurons are absent in numb- embryos and after ubiquitous expression of tramtrack, indicating that the activity of numb and the absence of tramtrack are required to produce both external sense organ and multidendritic neural fates. The analysis of string- embryos reveals that when the precursors are unable to divide they differentiate mostly into type II neurons, indicating that the type II is the default neuronal fate. We also report a new mutant phenotype where the ASC-dependent neurons are converted into type II neurons, providing evidence for the existence of one or more genes required for maintaining the alternative (type I) fate. Our results suggest that the same mechanism of type I/type II specification may operate at a late step of the ASC-dependent lineages, when multidendritic neurons arise as siblings of the external sense organ neurons and, at an early step, when other multidendritic neurons precursors arise as siblings of external sense organ precursors.

Fine structure of peripheral terminations in the porous sensillar cone of larvae of Ctenicera destructor (Brown) (Coleoptera, Elateridae), and probable fixation artifacts

1971 ◽  
Vol 49 (6) ◽  
pp. 789-799 ◽  
Author(s):  
R. Y. Zacharuk
Keyword(s):  
Fine Structure ◽  
Glutaraldehyde Fixation ◽  
Dendritic Branches ◽  
Peripheral Sensory ◽  
Ammoniacal Silver ◽  
Ctenicera Destructor

Nodes occur naturally on the dendritic branches in the receptor-lymph cavity of the antennal sensory cone in larvae of Ctenicera destructor. They increase in number, are often greatly expanded, and may separate from the dendrites as fixation artifacts. Extracellular dictyosomes originate from terminal nodes of the dendritic branches. These dictyosomes secrete vesicles, believed to contain lipoidal substances, directly into the fluid in the receptor cavity. These vesicles either coalesce into large lipoidal globules which produce the peripheral sensory tubules that traverse pores in the covering cuticle, or themselves attach directly to the tubules. The sensory tubules are lipoidal in nature. It is suggested that they serve to conserve moisture in the sensillum and to channel stimulating molecules through the cuticle to the lymph in the receptor cavity. The dendrites are not attached directly to the sensory tubules, but are believed to gain contact with the stimulating molecules through the receptor lymph. The lipoidal substance for sensory tubule secretion is probably transported into the sensory cone by the neurotubules within the dendrites. The results from a technique using glutaraldehyde fixation, ammoniacal silver treatment, and lead staining, without osmium fixation, are described and discussed.

scholarly journals Isolation and characterization of novel primary cells from the human distal outflow pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Uttio Roy Chowdhury ◽  
Cindy K. Bahler ◽  
Cheryl R. Hann ◽  
Bradley H. Holman ◽  
Michael P. Fautsch
Keyword(s):  
Trabecular Meshwork ◽  
Distal Region ◽  
Proximal Region ◽  
Cellular Growth ◽  
Model Systems ◽  
Type I ◽  
Isolation And Characterization ◽  
Outflow Pathway

AbstractOcular hypertension occurs due to increased resistance to aqueous humor removal through the conventional outflow pathway. Unlike the proximal region of the conventional outflow pathway, the distal region has not been well studied, mostly due to lack of model systems. Here we describe isolation and characterization of human primary vascular distal outflow pathway (VDOP) cells from the distal region of the conventional outflow pathway. Tissue from the distal region was isolated from human corneo-scleral rims, digested with collagenase type I (100 U/ml) and placed on gelatin coated plates to allow cellular growth in Dulbecco’s Modified Eagle’s Medium (low glucose) containing fetal bovine serum and antibiotic/antimycotic. VDOP cells showed consistent proliferation for up to 7 passages, retained endothelial-like nature of the parent tissues and showed a unique marker phenotype of Lectin+VEGFR2-CD34-NG2- that was distinct from neighboring trabecular meshwork (Lectin+VEGFR2-CD34-NG2+) and Schlemm’s canal (Lectin+VEGFR2+CD34+NG2+) cells. Dexamethasone treated VDOP cells did not express myocilin and did not form cross-linked actin networks, in contrast to trabecular meshwork cells. These data show that VDOP cells are unique to the distal outflow region and can be used as a viable in vitro model system to understand the biology of the distal outflow pathway and intraocular pressure regulation.

A C. elegans Hox gene switches on, off, on and off again to regulate proliferation, differentiation and morphogenesis

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1651-1661 ◽  
Author(s):  
S.J. Salser ◽  
C. Kenyon
Keyword(s):  
Cellular Response ◽  
Hox Genes ◽  
Sense Organ ◽  
Cellular Level ◽  
The Body ◽  
Body Region ◽  
Hox Gene ◽  
C Elegans ◽  
Independent Events ◽  
Gene Switches

Hox genes establish body pattern throughout the animal kingdom, but the role these genes play at the cellular level to modify and shape parts of the body remains a mystery. We find that the C. elegans Antennapedia homolog, mab-5, sequentially programs many independent events within individual cell lineages. In one body region, mab-5 first switches ON in a lineage to stimulate proliferation, then OFF to specify epidermal structures, then ON in just one branch of the lineage to promote neuroblast formation, and finally OFF to permit proper sense organ morphology. In a neighboring lineage, continuous mab-5 expression leads to a different pattern of development. Thus, this Hox gene achieves much of its power to diversify the anteroposterior axis through fine spatiotemporal differences in expression coupled with a changing pattern of cellular response.

scholarly journals Residues 28 to 39 of the Extracellular Loop 1 of Chicken Na+/H+ Exchanger Type I Mediate Cell Binding and Entry of Subgroup J Avian Leukosis Virus

2017 ◽  
Vol 92 (1) ◽  
Author(s):  
Xiaolu Guan ◽  
Yao Zhang ◽  
Mengmeng Yu ◽  
Chaoqi Ren ◽  
Yanni Gao ◽  
...  
Keyword(s):  
Avian Leukosis Virus ◽  
Proximal Region ◽  
Economic Losses ◽  
Cellular Receptor ◽  
Functional Domain ◽  
Type I ◽  
Receptor Function ◽  
Chimeric Receptors ◽  
Membrane Proximal Region ◽  
Subgroup J

ABSTRACTChicken Na+/H+exchanger type I (chNHE1), a multispan transmembrane protein, is a cellular receptor of the subgroup J avian leukosis virus (ALV-J). To identify the functional determinants of chNHE1 responsible for the ALV-J receptor activity, a series of chimeric receptors was created by exchanging the extracellular loops (ECL) of human NHE1 (huNHE1) and chNHE1 and by ECL replacement with a hemagglutinin (HA) tag. These chimeric receptors then were used in binding and entry assays to map the minimal ALV-J gp85-binding domain of chNHE1. We show that ECL1 of chNHE1 (chECL1) is the critical functional ECL that interacts directly with ALV-J gp85; ECL3 is also involved in ALV-J gp85 binding. Amino acid residues 28 to 39 of the N-terminal membrane-proximal region of chECL1 constitute the minimal domain required for chNHE1 binding of ALV-J gp85. These residues are sufficient to mediate viral entry into ALV-J nonpermissive cells. Point mutation analysis revealed that A30, V33, W38, and E39 of chECL1 are the key residues mediating the binding between chNHE1 and ALV-J gp85. Further, the replacement of residues 28 to 39 of huNHE1 with the corresponding chNHE1 residues converted the nonfunctional ALV-J receptor huNHE1 to a functional one. Importantly, soluble chECL1 and huECL1 harboring chNHE1 residues 28 to 39 both could effectively block ALV-J infection. Collectively, our findings indicate that residues 28 to 39 of chNHE1 constitute a domain that is critical for receptor function and mediate ALV-J entry.IMPORTANCEchNHE1 is a cellular receptor of ALV-J, a retrovirus that causes infections in chickens and serious economic losses in the poultry industry. Until now, the domains determining the chNHE1 receptor function remained unknown. We demonstrate that chECL1 is critical for receptor function, with residues 28 to 39 constituting the minimal functional domain responsible for chNHE1 binding of ALV-J gp85 and efficiently mediating ALV-J cell entry. These residues are located in the membrane-proximal region of the N terminus of chECL1, suggesting that the binding site of ALV-J gp85 on chNHE1 is probably located on the apex of the molecule; the receptor-binding mode might be different from that of retroviruses. We also found that soluble chECL1, as well as huECL1 harboring chNHE1 residues 28 to 39, effectively blocked ALV-J infection. These findings contribute to a better understanding of the ALV-J infection mechanism and also provide new insights into the control strategies for ALV-J infection.

scholarly journals Transcriptional regulation of the human TRIF (TIR domain-containing adaptor protein inducing interferon beta) gene

2004 ◽  
Vol 380 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Matthew P. HARDY ◽  
Anne F. McGETTRICK ◽  
Luke A. J. O'NEILL
Keyword(s):  
Interleukin 1 ◽  
Adaptor Protein ◽  
Inducible Promoter ◽  
Nuclear Factor Κb ◽  
Distal Region ◽  
Proximal Region ◽  
Type I ◽  
Gene Encoding ◽  
Interleukin 1Α ◽  
Factor Α

TRIF [TIR (Toll/interleukin-1 receptor) domain-containing adaptor protein inducing interferon β; also known as TICAM-1 (TIR-containing adaptor molecule-1)] is a key adaptor for TLR3 (Toll-like receptor 3)- and TLR4-mediated signalling. We have performed a detailed annotation of the human TRIF gene and fine analysis of the basal and inducible promoter elements lying 5´ to the site of initiation of transcription. Human TRIF maps to chromosome 19p13.3 and is flanked upstream by TIP47, which encodes the mannose 6-phosphate receptor binding protein, and downstream by a gene encoding FEM1a, a human homologue of the Caenorhabditis elegans Feminisation-1 gene. Using promoter–reporter deletion constructs, we identified a distal region with the ability to negatively regulate basal transcription and a proximal region containing an Sp1 (stimulating protein 1) site that confers approx. 75% of basal transcriptional activity. TRIF expression can be induced by multiple stimuli, such as the ligands for TLR2, TLR3 and TLR4, and by the pro-inflammatory cytokines tumour necrosis factor α and interleukin-1α. All of these stimuli act via an NF-κB (nuclear factor-κB) motif at position −127. In spite of the presence of a STAT1 (signal transduction and activators of transcription 1) motif at position −330, the addition of type I or type II interferon had no effect on TRIF activity. The human TRIF gene would therefore appear to be regulated primarily by NF-κB.

scholarly journals Identification of the invariant chain (CD74) as an angiotensin AGTR1-interacting protein

2008 ◽  
Vol 199 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Márta Szaszák ◽  
Hung-Dar Chen ◽  
Hao-Chia Chen ◽  
Albert Baukal ◽  
László Hunyady ◽  
...  
Keyword(s):  
Protein Interactions ◽  
Biosynthetic Pathway ◽  
Human Kidney ◽  
Proximal Region ◽  
Negative Regulator ◽  
Site Directed Mutagenesis ◽  
Invariant Chain ◽  
Type I ◽  
Interacting Protein ◽  
Carboxyl Terminal

Little is known about the protein–protein interactions that regulate the trafficking of the angiotensin II type I receptor (AGTR1) through the biosynthetic pathway. The membrane-proximal region of the cytoplasmic tail of the AGTR1 has been identified by site-directed mutagenesis studies as an essential site for normal AGTR1 folding and surface expression. Based on yeast two-hybrid screening of a human kidney cDNA library with the AGTR1 carboxyl-terminal tail as a bait, we identified the invariant chain (CD74) as a novel interacting protein. This association was confirmed by co-immunoprecipitation and co-localization studies. The binding site for CD74 on the AGTR1 carboxyl-terminal tail was localized to a site previously identified as important for the exit of the AGTR1 from the endoplasmic reticulum (ER), and conserved in many G protein-coupled receptors. Transient co-expression of CD74 with the AGTR1 in CHO-K1 cells consistently reduced the AGTR1 density at the cell surface. Furthermore, the interaction of CD74 with the carboxyl-terminal tail of the AGTR1 caused its retention in the ER and promoted its proteasomal degradation. These observations indicate that CD74 and the AGTR1 become associated in the early biosynthetic pathway, and that CD74 is a negative regulator of AGTR1 expression.

scholarly journals Experimental poisoning by Senecio brasiliensis in calves: quantitative and semi-quantitative study on changes in the hepatic extracellular matrix and sinusoidal cells

2008 ◽  
Vol 28 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Márcia Bersane A.M. Torres ◽  
Kunie I.R. Coelho
Keyword(s):  
Extracellular Matrix ◽  
Light Microscopy ◽  
Liver Damage ◽  
Elastic Fiber ◽  
Elastic Fibers ◽  
Type I ◽  
Collagen Types ◽  
Fiber System ◽  
Sinusoidal Cells ◽  
Total Collagen

Extracellular matrix plays an important role in chronic hepatic lesions and has been studied in experimental intoxication models. However in cattle, studies on chronic disease have focused on the hepatocellular damage and extracellular matrix (ECM) changes are usually overlooked. There are no specific studies on the hepatic ECM in either normal or chronically damaged bovine liver. Thus an experimental model of hepatic toxicity model using Senecio brasiliensis poisoned calves was designed. Senecio brasiliensis contains pyrrolizidine alkaloids which cause either acute or chronic progressive dose dependent liver damage. Five calves were orally fed with 0.38g of dry leaves of S. brasiliensis/kg/day for 24 days. Liver needle biopsy specimens were obtained every 15 days for 60 days. Clinical signs of digestive complications appeared at 3rd week. One calf died on 45th day and four were evaluated up to 60th day. Biopsy samples were processed for routine light microscopy, immuno-histochemistry and transmission electron microscopy. From 30th day on progressive liver damage characterized by hepatocellular ballooning, necrosis, apoptosis and megalocytosis, centrilobular, pericellular and portal fibrosis were seen by light microscopy. Quantitative and semi-quantitative measurements of hepatic ECM components were performed before and after the onset of lesions. Morphometric analysis of total collagen and elastic fiber system was conducted. Total collagen and I and III collagen types progressively increased in throughout the liver of affected calves. Changes in location, amount and disposition of the elastic fiber system were also observed. Then numbers of Kupffer cells were significantly increased at 30th day and total numbers of sinusoidal cells were significantly increased at 45th and 60th days. Liver damage was progressive and irreversible even after the exposure to the plant was discontinued. Severe fibrotic lesions occurred mainly in portal tracts, followed by veno-occlusive and pericellular fibrosis. Collagen types I and III s were present in every normal and damaged liver, with predominance of type I. In affected calves the increase of total collagen and elastic fibers system paralleled the number of total sinusoidal cells.

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