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Mutations in the clk-1 gene of Caenorhabditis elegans affect developmental and behavioral timing.

We have identified three allelic, maternal-effect mutations that affect developmental and behavioral timing in Caenorhabditis elegans. They result in a mean lengthening of embryonic and postembryonic development, the cell cycle period and life span, as well as the periods of the defecation, swimming and pumping cycles. These mutants also display a number of additional phenotypes related to timing. For example, the variability in the length of embryonic development is several times larger in the mutants than in the wild type, resulting in the occasional production of mutant embryos developing more rapidly than the most rapidly developing wild-type embryos. In addition, the duration of embryonic development of the mutants, but not of the wild type, depends on the temperature at which their parents were raised. Finally, individual variations in the severity of distinct mutant phenotypes are correlated in a counterintuitive way. For example, the animals with the shortest embryonic development have the longest defecation cycle and those with the longest embryonic development have the shortest defecation cycle. Most of the features affected by these mutations are believed to be controlled by biological clocks, and we therefore call the gene defined by these mutations clk-1, for "abnormal function of biological clocks."

Alleles↗

Poor centrosomal function of cat testicular spermatozoa impairs embryo development in vitro after intracytoplasmic sperm injection.

In the domestic cat, morula-blastocyst formation in vitro is compromised after intracytoplasmic sperm injection (ICSI) with testicular compared to ejaculated spermatozoa. The aim of this study was to determine the cellular basis of the lower developmental potential of testicular spermatozoa. Specifically, we examined the influence of sperm DNA fragmentation (evaluated by TUNEL assay) and centrosomal function (assessed by sperm aster formation after ICSI) on first-cleavage timing, developmental rate, and morula-blastocyst formation. Because the incidences of DNA fragmentation were not different between testicular and ejaculated sperm suspensions, DNA integrity was not the origin of the reduced developmental potential of testicular spermatozoa. After ICSI, proportions of fertilized and cleaved oocytes were similar and not influenced by sperm source. However, observations made at 5 h postactivation clearly demonstrated that 1) zygotes generally contained a large sperm aster after ICSI with ejaculated spermatozoa, a phenomenon never observed with testicular spermatozoa, and 2) proportions of zygotes with short or absent sperm asters were higher after ICSI with testicular spermatozoa than using ejaculated spermatozoa. The poor pattern of aster formation arose from the testicular sperm centrosome, which contributed to a delayed first cleavage, a slower developmental rate, and a reduced formation of morulae and blastocysts compared to ejaculated spermatozoa. When a testicular sperm centrosome was replaced by a centrosome from an ejaculated spermatozoon, kinetics of first cell cycle as well as embryo development quality significantly improved and were comparable to data from ejaculated spermatozoa. Results demonstrate for the first time in mammals that maturity of the cat sperm centrosome (likely via epididymal transit) contributes to an enhanced ability of the spermatozoon to produce embryos that develop normally to the morula and blastocyst stages.

Animals↗

Factors affecting the distribution of enamel hypoplasias within the human permanent dentition.

Frequencies and morphological and chronological distributions of enamel hypoplasias are presented by tooth type (permanent I1 to M2s), based on a sample of 30 prehistoric Amerindians with complete and unworn dentitions. There is nearly a tenfold variation in frequency of defects by tooth, ranging from 0.13 per mandibular second molar to 1.27 per maxillary central incisor. The six anterior teeth average between 0.70 and 1.27 defects/tooth, whereas the eight posterior teeth average between 0.43 and 0.13 defects/tooth. Earlier developing teeth, such as incisors, have earlier peak frequencies of defects (2.0-2.5 years), while later developing teeth, such as second molars, have subsequent peak frequencies (5.0-6.0 years). These variations are relevant when comparing hypoplasia data based on different teeth. Differences in hypoplasia frequencies among teeth are not solely due to variation in time of crown development, as is usually reported. Rather, there is evidence for biological gradients in susceptibility to ameloblastic disruption. Anterior teeth are more hypoplastic than posterior teeth. More developmentally stable "polar" teeth are more hypoplastic than surrounding teeth. Polar teeth may be more susceptible to hypoplasias because their developmental timing is less easily disrupted. In all teeth, hypoplasias are most common in the middle and cervical thirds. Crown development and morphological factors, such as enamel prism length and direction, may influence the development and expression of enamel surface defects.

Amelogenesis↗

Leukemia in twins: lessons in natural history.

Identical infant twins with concordant leukemia were first described in 1882, and since that time many such pairs of infants and older children have been described. It has long been recognized that this situation offers a unique opportunity to identify aspects of the developmental timing, natural history, and molecular genetics of pediatric leukemia in general. We reviewed both the older literature and more recent molecular biologic studies that have uncovered the basis of concordance of leukemia. Molecular markers of clonality, including unique, genomic fusion gene sequences, have provided unequivocal evidence that twin pairs of leukemia have a common clonal origin. The only plausible basis for this, first suggested more than 40 years ago, is that following initiation of leukemia in one twin fetus, clonal progeny spread to the co-twin via vascular anastomoses within a single, monochorionic placenta. This explanation has been endorsed by the identification of clonotypic gene fusion sequences in archived neonatal blood spots of individuals who subsequently developed leukemia. These analyses of twin leukemias have thrown considerable light on the natural history of disease. They reveal a frequent prenatal origin and an early or initiating role for chromosome translocations. Further, they provide evidence for a variable and often protracted latency and the need, in childhood acute lymphoblastic leukemia (ALL)/acute myeloblastic leukemia (AML), for further postnatal exposures and/or genetic events to produce clinical disease. We argue that these insights provide a very useful framework for attempts to understand etiologic mechanisms.

Humans↗

Survival of immature Anopheles arabiensis (Diptera: Culicidae) in aquatic habitats in Mwea rice irrigation scheme, central Kenya.

BACKGROUND: The survivorship and distribution of Anopheles arabiensis larvae and pupae was examined in a rice agro-ecosystem in Mwea Irrigation Scheme, central Kenya, from August 2005 to April 2006, prior to implementation of larval control programme. METHODS: Horizontal life tables were constructed for immatures in semi-field condition. The time spent in the various immature stages was determined and survival established. Vertical life tables were obtained from five paddies sampled by standard dipping technique. RESULTS: Pre-adult developmental time for An. arabiensis in the trays in the experimental set up in the screen house was 11.85 days from eclosion to emergence. The mean duration of each instar stage was estimated to be 1.40 days for first instars, 2.90 days for second instars, 1.85 days for third instars, 3.80 days for fourth instars and 1.90 days for pupae. A total of 590 individuals emerged into adults, giving an overall survivorship from L1 to adult emergence of 69.4%. A total of 4,956 An. arabiensis immatures were collected in 1,400 dips throughout the sampling period. Of these, 55.9% were collected during the tillering stage, 42.5% during the transplanting period and 1.6% during the land preparation stage. There was a significant difference in the An. arabiensis larval densities among the five stages. Also there was significant variation in immature stage composition for each day's collection in each paddy. These results indicate that the survival of the immatures was higher in some paddies than others. The mortality rate during the transplanting was 99.9% and at tillering was 96.6%, while the overall mortality was 98.3%. CONCLUSION: The survival of An. arabiensis immatures was better during the tillering stage of rice growth. Further the survival of immatures in rice fields is influenced by the rice agronomic activities including addition of nitrogenous fertilizers and pesticides. For effective integrated vector management, the application of larvicides should target An. arabiensis larvae at the tillering stage (early vegetative stage of rice) when their survival in the aquatic habitats is high to significantly reduce them and the larvicides should be long-lasting to have a significant impact on the malaria vector productivity on the habitats.

Animals↗

Colonic atresia without mesenteric vascular occlusion. The role of the fibroblast growth factor 10 signaling pathway.

BACKGROUND/PURPOSE: Colonic atresia occurs in 1:20,000 live births, offering a neonatal surgical challenge. Prenatal expression of fibroblast growth factor 10 (Fgf10), acting through fibroblast growth factor receptor 2b (Fgfr2b), is critical to the normal development of the colon. Invalidation of the Fgf10 pathway results in colonic atresia, inherited in an autosomal recessive pattern. Classically, disturbance of the mesenteric vasculature has been thought to cause many forms of intestinal atresia. The purpose of this study was to evaluate the role of vascular occlusion in the pathogenesis of colonic atresia. METHODS: Wild type (Wt), Fgf10(-/-), and Fgfr2b(-/-) mutant mouse embryos were harvested from timed pregnant mothers. Immediately following harvest, filtered India ink was infused via intracardiac microinjection. The gastrointestinal tract was dissected, and photomicrographs of the mesenteric arterial anatomy were taken at key developmental time points. RESULTS: Photomicrographs after India ink microinjections demonstrate normal, patent mesenteric cascades to the atretic colon at the time points corresponding to the failure of colonic development in the Fgf10(-/-) and Fgfr2b(-/-) mutants. The mesenteric arterial anatomy of the colon demonstrates no difference between the Wt and mutant colonic atresia. CONCLUSIONS: The absence of embryonic expression of Fgf10 or its receptor Fgfr2b results in colonic atresia in mice. India ink microinjection is a direct measure of mesenteric arterial patency. Colonic atresia in the Fgf10(-/-) and Fgfr2b(-/-) mutants occurs despite normal mesenteric vascular development. Thus the atresia is not the result of a mesenteric vascular occlusion. The patent colonic mesentery of the Fgf10(-/-) and Fgfr2b(-/-) mutants challenges an accepted pathogenesis of intestinal atresia. Although colonic atresia can occur as a result of vascular occlusion, new evidence exists to suggest that a genetic mechanism may play a role in the pathogenesis of this disease.

Animals↗

Aberrant folate response and premature development in a mutant of Dictyostelium discoideum.

Growth and development are mutually exclusive in Dictyostelium discoideum. The transition between the two stages of the life cycle is regulated by the relative abundance of nutrients and proteins secreted by the cells which reflect population density. At the transition from growth to development, the discoidin genes--developmental markers--are induced by the "quorum" protein PSF. The effect of PSF is counteracted by food bacteria and by folate [8]. We show that folate treatment during growth delays morphologic development. Furthermore, we demonstrate that in a mutant of Dictyostelium discoideum (V188, renamed HBW3), which expresses discoidinI during growth and which develops rapidly [46], discoidinI expression is less sensitive to folate than in wild type cells. Finally, we present evidence that fragments of the discoidinI gamma promoter which are unresponsive to PSF and CM are sufficient for misregulation in the mutant. The only known regulator of these promoter elements is folate. Changes in the expression of other early developmental genes are also shown. Taken together, these data suggest that the reduced sensitivity to folate might be the cause for the "rapid development" phenotype of the mutant and that folate regulates developmental timing.

3',5'-Cyclic-AMP Phosphodiesterases↗

Ontogenetic differences in the regional and cellular acetylcholinesterase and butyrylcholinesterase activity in the rat brain

Considering the novel functions for both acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in the developing nervous system (reviewed in Layer and Willbold, Prog. Histochem. Cytochem., 1995) a quantitative survey of the spatiotemporal developmental profiles of both AChE and BuChE activity in the neonatal rat brain would be extremely useful. To that end, we collected six brain regions at seven developmental time points, (postnatal day 1, 4, 7, 12, 17, 21, adult; n>/=3) and measured AChE and BuChE activity using both biochemical and histological methods. These results indicated that the developmental pattern of AChE and BuChE activity varied with respect to brain region and age: (1) the ontogeny of either AChE or BuChE specific activity in one region was not necessarily indicative of the developmental pattern of the same cholinesterase in other regions; (2) the AChE developmental profile in a given region did not necessarily predict the BuChE developmental pattern for that same region. The data were also analyzed from a different perspective, i.e., the ratio of BuChE-AChE activity, in order to determine if BuChE activity preceded AChE activity during development as has been proposed for the chick nervous system (Layer, Proc. Natl. Acad. Sci. USA, 1983). Our analysis showed that, in general, the BuChE-AChE ratio decreased as the region matured, data which parallel the pattern of development of these esterases in the chick nervous system.

Journal Article↗

Heart development in Drosophila requires the segment polarity gene wingless.

Mesoderm induction has been studied in many systems and some of the factors involved have been identified. Although the heart is mesodermal in origin, the molecular basis of heart development is essentially unknown. The Drosophila heart is a simple tubular structure similar to the early heart tube in vertebrates. The homeobox gene, tinman, has been shown to be crucial for heart formation in Drosophila. Several genes with considerable sequence similarities to tinman are expressed in cardiac primordial tissue of vertebrates and are likely to be required for heart development of higher organisms as well. In addition to transcriptional control factors, heart development might also depend on inductive signals. Here, we demonstrate that the gene wingless (wg), which is known to specify segmental polarity and neuroblast identity in Drosophila, has a novel role in mesoderm development: wg function is specifically required for heart development. A temperature-sensitive mutation of wg was used to inactivate wg function during precise developmental time periods. Elimination of wg function for a short time period after gastrulation results in the selective loss of heart precursors, without significantly affecting the formation of the body wall or visceral muscles, although some pattern defects are observed. This developmental requirement of wg for cardiac organogenesis is distinct from its function in segmentation and neurogenesis. We conclude that wg signaling is a crucial component of heart formation.

Animals↗

Activation of skeletal alpha-actin gene transcription: the cooperative formation of serum response factor-binding complexes over positive cis-acting promoter serum response elements displaces a negative-acting nuclear factor enriched in replicating myoblasts and nonmyogenic cells.

Three upstream CBAR cis-acting promoter elements, containing the inner core CC(A/T)6GG of the serum response element (SRE), are required for myogenic cell type-restricted expression of the avian skeletal alpha-actin gene (K.L. Chow and R.J. Schwartz, Mol. Cell. Biol. 10:528-538, 1990). These actin SRE elements display differential binding properties with two distinct nuclear proteins, serum response factor (SRF) and another factor described here as F-ACT1. SRF is able to bind to all actin SREs with various affinities. This multisite interaction is marked by cooperative binding events in that the two high-affinity proximal and distal SREs facilitate the weak central-site interaction with SRF, leading to the formation of a higher-order SRF-promoter complex. Functional analyses reveal that undisrupted multiple SRF-DNA interactions are absolutely essential for promoter activity in myogenic cells. F-ACT1, present at higher levels in nonmyogenic cells and replicating myoblasts than in myotubes, binds solely to the proximal SRE, and its binding is mutually exclusive with that of SRF owing to their overlapping base contacts. The cooperative promoter binding by SRF, however, can effectively displace prebound F-ACT1. In addition, an intact F-ACT1 binding site acts as a negative promoter element by restricting developmentally timed expression in myoblasts. F-ACT1 may therefore act as a repressor of skeletal alpha-actin gene transcription. This interplay between F-ACT1 and SRF may constitute a developmental as well as a physiologically regulated mechanism which modulates sarcomeric actin gene expression.

Actins↗

Ontogenetic differences in the regional and cellular acetylcholinesterase and butyrylcholinesterase activity in the rat brain.

Considering the novel functions for both acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in the developing nervous system (reviewed in Layer and Willbold, Prog. Histochem. Cytochem., 1995) a quantitative survey of the spatiotemporal developmental profiles of both AChE and BuChE activity in the neonatal rat brain would be extremely useful. To that end, we collected six brain regions at seven developmental time points, (postnatal day 1, 4, 7, 12, 17, 21, adult; n > or = 3) and measured AChE and BuChE activity using both biochemical and histological methods. These results indicated that the developmental pattern of AChE and BuChE activity varied with respect to brain region and age: (1) the ontogeny of either AChE or BuChE specific activity in one region was not necessarily indicative of the developmental pattern of the same cholinesterase in other regions; (2) the AChE developmental profile in a given region did not necessarily predict the BuChE developmental pattern for that same region. The data were also analyzed from a different perspective, i.e., the ratio of BuChE-AChE activity, in order to determine if BuChE activity preceded AChE activity during development as has been proposed for the chick nervous system (Layer, Proc. Natl. Acad. Sci. USA, 1983). Our analysis showed that, in general, the BuChE-AChE ratio decreased as the region matured, data which parallel the pattern of development of these esterases in the chick nervous system.

Acetylcholinesterase↗

A comparative study of embryonic development of some bird species with different patterns of postnatal growth.

Some studies show that birds with high postnatal growth rates (e.g. altricial species) are characterized by a rapid early development of "supply" organs, such as digestive organs. Birds with low postnatal growth rates (e.g. precocial species) exhibit a slower early development of these organs and a more rapid early development of other "demand" organs, such as brain, muscles, skeleton and feathers. To test whether these differences can be traced back to early embryonic development and whether they can be associated with changes in developmental timing, i.e. heterochrony, we compared embryos of the precocial quail and the altricial fieldfare, two bird species with low and high postnatal growth rates, respectively. We used classical staging techniques that use developmental landmarks to categorize embryonic maturity as well as morphological measurements. These techniques were combined with immune detection of muscle specific proteins in the somites. Our data showed that the anlagen of the head, brain and eyes develop earlier in the quail than in the fieldfare in contrast to the gut which develops earlier in the fieldfare than in the quail. Our data also showed that the quail and the fieldfare displayed different rates of myotome formation in the somites which contribute to muscle formation in the limbs and thorax. We believe these observations are connected with important differences in neonatal characteristics, such as the size of the brain, eyes, organs for locomotion and digestion. This leads us to the conclusion that selection for late ontogenetic characteristics can alter early embryonic development and that growth rate is of fundamental importance for the patterning of avian embryonic development. It also appears that this comparative system offers excellent opportunities to test hypotheses about heterochrony.

Analysis of Variance↗

Effects of water quality on the vector competence of Culex tarsalis (Diptera: Culicidae) for western equine encephalomyelitis (Togaviridae) and St. Louis encephalitis (Flaviviridae) viruses.

The effects of water quality during immature development on the vector competence of adult female Culex tarsalis Coquillett for western equine encephalomyelitis (WEE) and St. Louis encephalitis (SLE) viruses was evaluated during 6 field and 4 laboratory experiments. Immatures of the Bakersfield Field Station laboratory strain and the F1 progeny of field-collected females were reared in the field or laboratory and then infected by feeding on pledgets, after which remnants (head, thorax, abdomen), legs, and salivary secretions were tested for WEE or SLE virus to estimate infection, dissemination, and transmission rates, respectively. Although the salt content of the 6 larval habitats varied markedly (range, alkalinity 160-1,310 ppm CaCO3, conductivity 460-7,600 microns hos/cm, chlorides 22-1,560 ppm) and significantly altered immature survival, development time, and female body size (wing length), consistent changes in infection, dissemination, or transmission rates were not observed. Susceptibility (ID50) to WEE virus in field strains decreased as a linear function of developmental time, with populations from a dry alkali lake bed (Goose Lake) least susceptible. Three subsequent laboratory experiments that tested the effects of rearing immatures in dilution series of water from Goose Lake failed to produce consistent within or among experiment patterns in vector competence. A 4th laboratory experiment tested changes in NaCl concentration with negative results. Changes in female size was not related to vector competence. These and previous temperature studies indicated that temporal changes in vector competence observed within and among field populations probably were related to intrinsic genetic factors and were not related directly to extrinsic factors in the immature aquatic environment.

Animals↗

Changes of hippocampal protein levels during postnatal brain development in the rat.

Information on postnatal brain protein expression is very limited, and we therefore compared hippocampal protein levels in rat hippocampus at different developmental time points using two-dimensional gel electrophoresis followed by mass spectrometrical protein identification and specific software for quantification. Proteins from several cascades as e.g., antioxidant, metabolic, cytoskeleton, proteasomal, and chaperone pathways were developmentally regulated, which is relevant for design and interpretation of protein chemical studies in the mammalian brain.

Aging↗

Effects of temperature on Chrysomya rufifacies (Diptera:Calliphoridae) development.

Growth curves were studied for the egg, larva, and pupa of Chrysomya rufifacies (Macquart) under mean cyclic temperatures of 15.6, 21.1, 26.7, and 35.0 degrees C and a constant temperature of 25.0 degrees C. Development from egg to adult under all regimes ranged from 190 to 598 h. A constant temperature of 25 degrees C produced a range of pupation times from 134 to 162 h, with adult emergence ranging from 237 to 289 h. The maximal preferential temperature of 35.1 degrees C was determined for maggots using a gradient system. Highly predictable developmental time, minimal larval length variation, and low cohort variation emphasize the utility of this species in entomological-based postmortem interval determinations. Therefore, C. rufifacies should be of primary forensic importance when recovered alone or in conjunction with other species of Calliphoridae.

Animals↗

Proper developmental control of human globin genes reproduced by transgenic mice containing a 160-kb BAC carrying the human beta-globin locus.

Four independent bacterial artificial chromosome (BAC) clones containing the human Beta-globin gene locus were obtained from a human genomic BAC library. A 160-kb clone (186D7) carrying the entire human Beta-globin locus including the Beta-globin gene family, locus control region (LCR), and 3' regulatory elements was used to transform mice. Four transgenic lines were generated by microinjecting the purified BAC DNA into the fertilized eggs. RNase protection analysis showed that the expression of human Beta-globin genes is tissue- and developmental stage-specific and the expression level is similar among the three independent transgenic lines which carry the entire human Beta-globin locus; however, no Beta-globin gene expression was detected in the transgenic mice lacking the LCR region. The results suggest that the transgenic mouse model system that we have produced and that uses BAC to study the complex human Beta-globin gene cluster is stable and reproducible. Our results also indicate that some newly characterized HSs upstream from the LCR appear not to play an important role in globin gene expression and switching, while the traditional LCR can ensure correct human Beta-globin gene expression in transgenic mice. The BAC-mediated transgenic system can be used for further studies to determine which kinds of cis-acting elements are included in regulating the developmental timing and the level of human Beta-globin gene expression.

Animals↗

The quest for genes causing complex traits in ocular medicine: successes, interpretations, and challenges.

Gene mapping and positional cloning have gained acceptance as state-of-the-art methods to identify molecules that cause common complex diseases. However, the use of specialized technology, varying study designs, and misconceptions about the role of novel findings in genetics has led to confusion among basic scientists and health care professionals alike regarding the importance of these findings in molecular diagnostics and individualized medicine. To alleviate this confusion, the successes achieved in the past few years in mapping of genes for complex traits such as age-related macular degeneration and glaucoma are interpreted in the context of the appropriate population biology framework. The current article veers away from propagating the overly simplistic belief of a linear relationship between a specific gene and age-related macular degeneration, particularly one that equates possession of a specific risk allele as the only precursor to end-stage disease. Ascribing predictive properties to a single gene without consideration of its network partners, timing of action, or environmental correlates argues for a static view of gene action. Modern viewpoints of the mechanisms of action of a gene are contextual and encompass more cohesive frameworks, ranging from the developmental timing of action, to the genomic and environmental milieu. In this regard, gene mapping studies that have been so immensely successful in the gene detection phase of a study provide biased perspectives on the importance of these genes and the corresponding risk alleles in the general population because of their limited sample size and constrained design. To move the field of gene-based diagnosis forward, it will be necessary to conduct additional cohort and longitudinal studies using the original gene finding studies as a knowledge base to develop predictive models. In summary, while we have achieved great successes in finding genes for complex traits, the application of these findings to clinical medicine is not straightforward. The key question of who will develop disease in the future remains.

Chromosome Mapping↗

The role of allatostatic and allatotropic neuropeptides in the regulation of juvenile hormone biosynthesis in Lacanobia oleracea (Lepidoptera: Noctuidae).

In the sphinghid moth Manduca sexta, two allatoactive neuropeptides appear to be responsible for regulating juvenile hormone (JH) production by the corpora allata (CA). These peptides (M. sexta allatostatin, Mas-AS, and M. sexta allatotropin, Mas-AT) respectively inhibit and stimulate in vitro JH biosynthesis by CA in this insect. However, although Mas-AS inhibits CA in both larval and adult insects, Mas-AT is active only in adult M. sexta. The situation in other lepidopteran species is less clear-cut and, although both peptides have been detected (usually by immunologic and/or molecular techniques) in several other moths (including noctuids), their function as regulators of JH production remains uncertain. In the tomato moth Lacanobia oleracea (Lepidoptera: Noctuidae), we have previously demonstrated the occurrence of Mas-AS and/or Mas-AT in extracts of CA, brain and other organs, and have shown that both peptides are present in larval and adult forms. However, in L. oleracea, although Mas-AS inhibits larval and adult CA in vitro, it does so only at relatively high concentrations, and to a maximum of only approximately 70%. By contrast, Mas-AT (which is also present in larval and adult L. oleracea) stimulates larval and adult CA, but is substantially more potent ( approximately 100 fold) than the allatostatin. In this paper we present the results of paired, concurrent measurements (using ELISA) of levels of Mas-AS and Mas-AT in brains, CA and hemolymph (plasma and hemocytes) of L. oleracea at times when there are marked changes in JH titers. We also present data on the in vitro rates of JH biosynthesis by isolated CA, and on hemolymph JH esterase activity measured at the same critical developmental times, and discuss all of these data in relation to the putative allatoregulatory roles of the M. sexta allatotropic and allatostatic neuropeptides in L. oleracea.

Animals↗