Octopod, a homeotic mutation of the moth Manduca sexta, influences the fate of identifiable pattern elements within the CNS

Development ◽  
1989 ◽  
Vol 105 (3) ◽  
pp. 621-628 ◽  
Author(s):  
R. Booker ◽  
J.W. Truman
Keyword(s):  
Central Nervous System ◽  
Manduca Sexta ◽  
Ventral Surface ◽  
Wild Type ◽  
The Central Nervous System ◽  
Homeotic Mutation ◽  
Thoracic Legs ◽  
Homeotic Mutations ◽  
Anterior Direction ◽  
Slight Deformation

Octopod (Octo) is a mutation of the moth Manduca sexta, which results in the homeotic transformation of the ventral surface of the first (A1) and less often the second (A2) abdominal segments in the anterior direction. The extent of the transformation ranges from a slight deformation of the ventral cuticle, up to the formation of miniature thoracic legs on A1. The extent of the transformation is always less within A2 as compared to A1. A genetic analysis revealed that Octo is an autosomal mutation which shows incomplete dominance. The effect of this mutation on the central nervous system (CNS) was assessed by examining the distribution and fate of the postembryonic neuroblasts in the segmental ganglia of Octo larvae. In each of the thoracic ganglia of wild-type larvae, there is a set of 45–47 neuroblasts; a reduced but homologous array of 24 and 10 neuroblasts are found in A1 and A2, respectively. Ganglion A1 of Octo larvae had 1 to 6 supernumerary neuroblasts, and 20% of the A2 ganglia showed a single ectopic neuroblast. The supernumerary neuroblasts corresponded to identifiable neuroblasts normally found in more anterior ganglia. The Octo mutation also influenced the mitotic activity of stem cells normally present in A1. In this case, the neuroblasts generated a lineage of cells that were typical of a thoracic location rather than A1. These data demonstrate that homeotic mutations can influence the fate of identifiable pattern elements within the CNS of an insect.

The Larval Eclosion Hormone Neurones in Manduca Sexta: Identification of the Brain-Proctodeal Neurosecretory System

1989 ◽  
Vol 147 (1) ◽  
pp. 457-470 ◽  
Author(s):  
JAMES W. TRUMAN ◽  
PHILIP F. COPENHAVER
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Nerve Cord ◽  
Release Site ◽  
Neurosecretory System ◽  
Nerve Activity ◽  
Eclosion Hormone ◽  
The Central Nervous System ◽  
The Brain

Larval and pupal ecdyses of the moth Manduca sexta are triggered by eclosion hormone (EH) released from the ventral nervous system. The major store of EH activity in the latter resides in the proctodeal nerves that extend along the larval hindgut. At pupal ecdysis, the proctodeal nerves show a 90% depletion of stored activity, suggesting that they are the major release site for the circulating EH that causes ecdysis. Surgical experiments involving the transection of the nerve cord or removal of parts of the brain showed that the proctodeal nerve activity originates from the brain. Retrograde and anterograde cobalt fills and immunocytochemistry using antibodies against EH revealed two pairs of neurons that reside in the ventromedial region of the brain and whose axons travel ipsilaterally along the length of the central nervous system (CNS) and project into the proctodeal nerve, where they show varicose release sites. These neurons constitute a novel neuroendocrine pathway in insects which appears to be dedicated solely to the release of EH.

Adipokinetic hormone stimulates neurones in the insect central nervous system.

1995 ◽  
Vol 198 (6) ◽  
pp. 1307-1311
Author(s):  
J J Milde ◽  
R Ziegler ◽  
M Wallstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Central Action ◽  
Adipokinetic Hormone ◽  
Metabolic Functions ◽  
Simple Preparation ◽  
Pressure Injection ◽  
The Central Nervous System ◽  
Insect Central Nervous System

A simple preparation designed to screen and compare the central action of putative neuroactive agents in the moth Manduca sexta is described. This approach combines microinjections into the central nervous system with myograms recorded from a pair of spontaneously active mesothoracic muscles. Pressure injection of either octopamine or Manduca adipokinetic hormone (M-AKH) into the mesothoracic neuropile increases the monitored motor activity. Under the conditions used, the excitatory effects of M-AKH exceed those of the potent neuromodulator octopamine. This suggests that M-AKH plays a role in the central nervous system in addition to its known metabolic functions and supports recent evidence that neuropeptides in insects can be multifunctional.

Degeneration of skeletal muscle, peripheral nerves, and the central nervous system in transgenic mice overexpressing wild-type prion proteins

Cell ◽  
1994 ◽  
Vol 76 (1) ◽  
pp. 117-129 ◽  
Author(s):  
David Westaway ◽  
Stephen J. DeArmond ◽  
Juliana Cayetano-Canlas ◽  
Darlene Groth ◽  
Dallas Foster ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Transgenic Mice ◽  
Peripheral Nerves ◽  
Prion Proteins ◽  
Wild Type ◽  
The Central Nervous System

scholarly journals Delayed development of specific thyroid hormone-regulated events in transthyretin null mice

2013 ◽  
Vol 304 (1) ◽  
pp. E23-E31 ◽  
Author(s):  
Julie A. Monk ◽  
Natalie A. Sims ◽  
Katarzyna M. Dziegielewska ◽  
Roy E. Weiss ◽  
Robert G. Ramsay ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Thyroid Hormone ◽  
Bone Growth ◽  
Circulatory System ◽  
Goblet Cells ◽  
Wild Type ◽  
The Central Nervous System ◽  
Delayed Growth

Thyroid hormones (THs) are vital for normal postnatal development. Extracellular TH distributor proteins create an intravascular reservoir of THs. Transthyretin (TTR) is a TH distributor protein in the circulatory system and is the only TH distributor protein synthesized in the central nervous system. We investigated the phenotype of TTR null mice during development. Total and free 3′,5′,3,5-tetraiodo-l-thyronine (T4) and free 3′,3,5-triiodo-l-thyronine (T3) in plasma were significantly reduced in 14-day-old (P14) TTR null mice. TTR null mice also displayed a delayed suckling-to-weaning transition, decreased muscle mass, delayed growth, and retarded longitudinal bone growth. In addition, ileums from postnatal day 0 (P0) TTR null mice displayed disordered architecture and contained fewer goblet cells than wild type. Protein concentrations in cerebrospinal fluid from P0 and P14 TTR null mice were higher than in age-matched wild-type mice. In contrast to the current literature based on analyses of adult TTR null mice, our results demonstrate that TTR has an important and nonredundant role in influencing the development of several organs.

scholarly journals Borna Disease Virus Accelerates Inflammation and Disease Associated with Transgenic Expression of Interleukin-12 in the Central Nervous System

2002 ◽  
Vol 76 (23) ◽  
pp. 12223-12232 ◽  
Author(s):  
Susanna Freude ◽  
Jürgen Hausmann ◽  
Markus Hofer ◽  
Ngan Pham-Mitchell ◽  
Iain L. Campbell ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transgenic Mice ◽  
Disease Virus ◽  
Biologically Active ◽  
Interleukin 12 ◽  
Wild Type ◽  
Borna Disease Virus ◽  
The Central Nervous System ◽  
Borna Disease

ABSTRACT Targeted expression of biologically active interleukin-12 (IL-12) in astrocytes of the central nervous system (CNS) results in spontaneous neuroimmunological disease of aged mice. Borna disease virus (BDV) can readily multiply in the mouse CNS but does not trigger disease in most strains. Here we show that a large percentage of IL-12 transgenic mice developed severe ataxia within 5 to 10 weeks after infection with BDV. By contrast, no disease developed in mock-infected IL-12 transgenic and wild-type mice until 4 months of age. Neurological symptoms were rare in infected wild-type animals, and if they occurred, these were milder and appeared later. Histological analyses showed that the cerebellum of infected IL-12 transgenic mice, which is the brain region with strongest transgene expression, contained large numbers of CD4+ and CD8+ T cells as well as lower numbers of B cells, whereas other parts of the CNS showed only mild infiltration by lymphocytes. The cerebellum of diseased mice further showed severe astrogliosis, calcifications and signs of neurodegeneration. BDV antigen and nucleic acids were present in lower amounts in the inflamed cerebellum of infected transgenic mice than in the noninflamed cerebellum of infected wild-type littermates, suggesting that IL-12 or IL-12-induced cytokines exhibited antiviral activity. We propose that BDV infection accelerates the frequency by which immune cells such as lymphocytes and NK cells enter the CNS and then respond to IL-12 present in the local milieu causing disease. Our results illustrate that infection of the CNS with a virus that is benign in certain hosts can be harmful in such normally disease-resistant hosts if the tissue is unfavorably preconditioned by proinflammatory cytokines.

Excitatory and inhibitory roles of central ganglia in initiation of the insect ecdysis behavioural sequence

2000 ◽  
Vol 203 (8) ◽  
pp. 1329-1340 ◽  
Author(s):  
D. Zitnan ◽  
M.E. Adams
Keyword(s):  
Neural Network ◽  
Central Nervous System ◽  
Nervous System ◽  
Manduca Sexta ◽  
Abdominal Ganglion ◽  
Suboesophageal Ganglion ◽  
Eclosion Hormone ◽  
The Central Nervous System ◽  
Inka Cells ◽  
Behavioural Sequence

Insects shed their old cuticle by performing the ecdysis behavioural sequence. To activate each subunit of this set of programmed behaviours in Manduca sexta, specific central ganglia are targeted by pre-ecdysis-triggering (PETH) and ecdysis-triggering (ETH) hormones secreted from Inka cells. PETH and ETH act on each abdominal ganglion to initiate, within a few minutes, pre-ecdysis I and II, respectively. Shortly thereafter, ETH targets the tritocerebrum and suboesophageal ganglion to activate the ecdysis neural network in abdominal ganglia through the elevation of cyclic GMP (cGMP) levels. However, the onset of ecdysis behaviour is delayed by inhibitory factor(s) from the cephalic and thoracic ganglia. The switch from pre-ecdysis to ecdysis is controlled by an independent clock in each abdominal ganglion and is considerably accelerated after removal of the head and thorax. Eclosion hormone (EH) appears to be one of the central signals inducing elevation of cGMP levels and ecdysis, but these actions are quite variable and usually restricted to anterior ganglia. EH treatment of desheathed ganglia also elicits strong production of cGMP in intact ganglia, suggesting that this induction occurs via the release of additional downstream factors. Our data suggest that the initiation of pre-ecdysis and the transition to ecdysis are regulated by stimulatory and inhibitory factors released within the central nervous system after the initial actions of PETH and ETH.

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