Larval fat body cells die during the early pupal stage in the frame of metamorphosis remodelation in Bombyx mori. J Insect Physiol
Division of Life Sciences, Graduate School of Natural Science and Technology, Kanazawa University, Kakumamachi, Kanazawa 920-1192, Japan. Journal of insect physiology
(Impact Factor: 2.47).
12/2011; 57(12):1715-22. DOI: 10.1016/j.jinsphys.2011.09.013
In holometabolus insects, morphology of the larval fat body is remodeled during metamorphosis. In higher Diptera, remodeling of the fat body is achieved by cell death of larval fat body cells and differentiation of the adult fat body from primordial cells. However, little is known about remodeling of the fat body at pupal metamorphosis in Lepidoptera. In this study, we found that cell death of the larval fat body in Bombyx mori occurs at shortly after pupation. About 30% of the fat body cells underwent cell death on days 1 and 2 after pupation. The cell death involved genomic DNA fragmentation, a characteristic of apoptosis. Surgical manipulation and in vitro culture of fat body cells revealed that 20-hydroxyecdysone and juvenile hormone had no effect on either initiation or progression of cell death. During cell death, a large increase in activity of caspase-3, a key enzyme of cell death, was observed. Western blot analysis of the active form of caspase-3-like protein revealed that the length of caspase-3 of B. mori was much larger than that of caspase-3 in other species. The results suggest that larval fat body cells of B. mori are removed through cell death, which is mediated by a caspase probably categorized in a novel family.
Available from: José Eduardo Serrão
- "In the fifth instar larvae of the lepidopteran, Manduca sexta, no apoptosis is observed in the fat body cells (Muller et al. 2004). Further, in B. mori, many fat body cells show apoptotic cell death in the early pupal stage (Kaneko et al. 2011). In D. melanogaster, immediately following pupation, the fat body cells detach from the organ persist throughout the development, and only some got removed through apoptosis (Aguila et al. 2007; Nelliot et al. 2006). "
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ABSTRACT: Fat body, typically comprising trophocytes, provides energy during metamorphosis. The fat body can be renewed once the larval phase is complete or recycled and relocated to form the fat body of the adult insect. This study aims to identify the class of programmed cell death that occurs within the fat body cells during the metamorphosis of the stingless bee Melipona quadrifasciata. Using immunodetection techniques, the fat body of the post-defecating larvae and the white-, pink-, brown-, and black-eyed pupae were tested for cleaved caspase-3 and DNA integrity, followed by ultrastructural analysis and identification of autophagy using RT-PCR for the Atg1 gene. The fat body of M. quadrifasciata showed some apoptotic cells positive for cleaved caspase-3, although without DNA fragmentation. During development, the fat body cells revealed an increased number of mitochondria and free ribosomes, in addition to higher amounts of autophagy Atg1 mRNA, than that of the pupae. The fat body of M. quadrifasciata showed few cells which underwent apoptosis, but there was evidence of increased autophagy at the completion of the larval stage. All together, these data show that some fat body cells persist during metamorphosis in the stingless bee M. quadrifasciata.
Protoplasma 10/2014; 252(2). DOI:10.1007/s00709-014-0707-z · 2.65 Impact Factor
Available from: Arnold De Loof
- "fect , namely programmed cell death in selected tissues , appears shortly after JH disappears from the body . Although a causal link seems plausible , it is surprising that the literature that causally links absence of JH to apoptosis is rather scarce . From the fact that in holometabolous insects ( in particular in higher Diptera ) the fat body ( Kaneko et al . , 2011 ) and midgut ( Cai et al . , 2012 ) disintegrate , it can be inferred that some mecha - nism initiates a death signal that ultimately ends in the irreversible collapse of the transmembrane potential / ionic gradient . Which mechanism causes such electrical failure ? Supernumerary larvae or abnormal , but still temporarily viable larval "
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ABSTRACT: In holometabolous insects the fall to zero of the titer of Juvenile Hormone ends its still poorly understood "status quo" mode of action in larvae. Concurrently it initiates metamorphosis of which the programmed cell death of all internal tissues that actively secrete proteins, such as the fat body, midgut, salivary glands, prothoracic glands etc is the most drastic aspect. These tissues have a very well developed rough endoplasmic reticulum, a known storage site of intracellular Ca(2+). A persistent high [Ca(2+)]i is toxic, lethal and causal to apoptosis. Metamorphosis becomes a logical phenomenon if analyzed from: 1. the causal link between calcium toxicity and apoptosis; 2. the largely overlooked fact that at least some isoforms of Ca(2+)-ATPases have a binding site for farnesol-like endogenous sesquiterpenoids (FRS). The Ca(2+)-ATPase blocker thapsigargin, like JH a sesquiterpenoid derivative, illustrates how absence of JH might work. The Ca(2+)-homeostasis system is concurrently extremely well conserved in evolution and highly variable, enabling tissue-, developmental-, and species specificity. As long as JH succeeds in keeping [Ca(2+)]i low by keeping the Ca(2+)-ATPases pumping, it acts as the " the status quo" hormone. When it disappears, its various inhibitory effects are lifted. The electrical wiring system of cells, in particular in the regenerating tissues, is subject to change during metamorphosis. The possibility is discussed that in vertebrates an endogenous farnesol-like sesquiterpenoid, probably farnesol itself, acts as a functional, but hitherto completely overlooked Juvenile anti-aging "Inbrome", a novel concept in signaling.
General and Comparative Endocrinology 01/2014; 199. DOI:10.1016/j.ygcen.2014.01.009 · 2.47 Impact Factor
Available from: jeb.biologists.org
- "The mechanisms by which larval energy reservoirs are tagged and then released for use in later developmental stages, and by which they are allocated for somatic maintenance and reproduction, are not well understood, but programmed cell death (PCD) or autophagy of the larval fat cells appear to be involved. In the silkworm moth Bombyx mori, PCD begins in the early pupal stage (Kaneko et al., 2011), when egg maturation occurs. A different process occurs during metamorphosis of the skipper butterfly, Calpodes ethlius. "
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ABSTRACT: Within the complex life cycle of holometabolous insects, nutritional resources acquired during larval feeding are utilized by the pupa and the adult. The broad features of the transfer of larval resources to the pupae and the allocation of larval resources in the adult have been described by studies measuring and tracking macronutrients at different developmental stages. However, the mechanisms of resource transfer from the larva and the factors regulating the allocation of these resources in the adult between growth, reproduction and somatic maintenance are unknown. Drosophila melanogaster Meigen presents a tractable system to test cellular/tissue mechanisms of resource acquisition and allocation, because of the detailed understanding of D. melanogaster development and the experimental tools to manipulate its tissues across developmental stages. In previous work, we demonstrated that the fat body of D. melanogaster larval is important for surviving starvation stress in the young adult and suggested that programmed cell death of the larval fat cells in the adult is important for allocation of resources for female reproduction. Here, we describe the temporal uptake of larval-derived carbon by the ovaries, and demonstrate the importance of larval fat-cell death in the maturation of the ovary and in fecundity. Larvae and adults were fed stable carbon isotopes to follow the acquisition of larval-derived carbon by the adult ovaries. We determined that over half of the nutrients acquired by the ovaries in 2-day old adult females are dependent upon the death of the fat cells. Furthermore, when programmed cell death is inhibited in the larval fat cells, ovarian development was depressed and fecundity reduced.
Journal of Experimental Biology 10/2012; 216(3). DOI:10.1242/jeb.078311 · 2.90 Impact Factor
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