org Interactive Fly, Drosophila dunce: Biological Overview | Evolutionary Homologs | Regulation | Developmental Biology | Effects of Mutation | References

Gene name - dunce

Synonyms -

Cytological map position - 3C11D4

Function - degrades c-AMP

Keywords - c-AMP pathway - learning pathway. calcium dependent enzymes

Symbol - dnc

FlyBase ID:FBgn0000479

Genetic map position - 1-3.9

Classification - c-AMP phosphodiesterase

Cellular location - cytoplasmic

NCBI links: Precomputed BLAST | Entrez Gene
Recent literature
Xiao, C. and Robertson, R.M. (2017). White-cGMP interaction promotes fast locomotor recovery from anoxia in adult Drosophila. PLoS One 12: e0168361. PubMed ID: 28060942
Increasing evidence indicates that the white (w) gene in Drosophila possesses extra-retinal functions in addition to its classical role in eye pigmentation. It has been previously shown that w+ promotes fast and consistent locomotor recovery from anoxia, but how w+ modulates locomotor recovery is largely unknown. This study shows that in the absence of w+, several PDE mutants, especially cyclic guanosine monophosphate (cGMP)-specific PDE mutants, display wildtype-like fast locomotor recovery from anoxia, and that during the night time, locomotor recovery is light-sensitive in white-eyed mutant w1118, and light-insensitive in PDE mutants under w1118 background. Data indicate the involvement of cGMP in the modulation of recovery timing and presumably, light-evoked cGMP fluctuation is associated with light sensitivity of locomotor recovery. This is further supported by the observations that w-RNAi-induced delay of locomotor recovery is completely eliminated by upregulation of cGMP through multiple approaches, including PDE mutation, simultaneous overexpression of an atypical soluble guanylyl cyclase Gyc88E, or sildenafil feeding. Lastly, prolonged sildenafil feeding promotes fast locomotor recovery from anoxia in w1118. Taken together, these data suggest that a White-cGMP interaction modulates the timing of locomotor recovery from anoxia.


The genetic dissection of learning and memory in Drosophila is two decades old. Recently, a great deal of progress has been made towards isolating new mutants as well as a better understanding of those originally isolated. Nighorn's paper reviews the recent developments in the understanding of the structure and function of the gene identified by the first and best-characterized of these mutants, the Drosophila dunce mutant (Nighorn, 1994). R. L. Davis (1996) provides an even more recent review.

Learning in flies is studied using an operant conditioning paradigm involving electric shock and olfactory cues. First an odor (the conditioned stimulus) is paired with electric shock (the unconditioned stimulus). The aversive effects of the shock teach the flies to avoid the odor, or as researchers tend to express it, avoidance of the conditioned stimuli is enhanced. Behavior attributable to learning is measured by testing with a second and different odor. Flies that have learned continue to avoid the conditioned stimulus but not the control odor, both in the absence of the unconditioned stimulus. Proper control includes a second experimental phase: employing the second odor as the conditioned stimulus. When paired with the shock, flies should then avoid the second (control) odor as they did the original conditioned stimulus (Quinn, 1972).

Cyclic AMP has been implicated as the mediator of learning in classical experiments using the marine snail Aplasia (Kandel, 1992). In this system, conditioned stimuli increased Ca++ concentration within neurons. The Ca++ binds to Calmodulin, which in turn binds to adenylate cylase, enhancing the ability of adenylate cyclase to synthesize c-AMP. The Drosophila adenyl cyclase homolog is rutabaga. Mutations in rut result in defective learning. A second gene, dunce, encodes the cAMP phosphodiesterase, the enzyme that degrades cAMP. Mutations in dunce also result in a learning deficit but when combined with the rut mutations in the same fly, the learning defect is reversed. At least in this case it appears that two wrongs make a right. It has been suggested that lower cAMP levels still result in learning despite the double mutation because the cAMP is degraded more slowly.

Protein kinase A, the target of cAMP signaling is a third protein involved in learning . PKA, activated by cAMP, initiates a phosphorylation cascade that in turn activates genes involved in the creation of long term memory. dCREB2, the cyclic AMP response element binding protein is one such gene, a transcription factor associated with long term memory. The Dfos and DJUN genes in Drosophila both have binding sites for CREB, while in mammals, only the fos promoter binds CREB (Davis, 1995, Fagnon, 1995 and Nighorn, 1994). For a discussion of the cellular basis of learning see the rutabaga site.

A novel bioassay system is described that uses Xenopus embryonic myocytes (myoballs) to detect the release of acetylcholine from Drosophila CNS neurons. When a voltage-clamped Xenopus myoball is manipulated into contact with cultured Drosophila 'giant' neurons, spontaneous synaptic current-like events are registered. These events are observed within seconds after contact and are blocked by curare and alpha-bungarotoxin, but not by TTX and Cd2+, suggesting that they are caused by the spontaneous quantal release of acetylcholine (ACh). The secretion occurs not only at the growth cone, but also along the neurite and at the soma, with significantly different release parameters among various regions. The amplitude of these currents displays a skewed distribution. These features are distinct from synaptic transmission at more mature synapses or autapses (a synapse between an axon collateral of a neuron and one of the same neuron's dendrites) formed in this culture system and are reminiscent of the transmitter release process during early development in other preparations. The usefulness of this coculture system in studying presynaptic secretion mechanisms is illustrated by a series of studies on the cAMP pathway mutations, dunce (dnc) and PKA-RI that disrupt a cAMP-specific phosphodiesterase and the regulatory subunit of cAMP-dependent protein kinase A, respectively. These mutations affect the ACh current kinetics, but not the quantal ACh packet, and the release frequency is greatly enhanced by repetitive neuronal activity in dnc, but not wild-type, growth cones. These results suggest that the cAMP pathway plays an important role in the activity-dependent regulation of transmitter release not only in mature synapses as previously shown, but also in developing nerve terminals before synaptogenesis (Yao, 2000).

It is now well established that Drosophila neurons share many molecular components of the transmitter release machinery with vertebrate neurons. The release of neurotransmitter is a multistep process that involves actions of proteins associated with the synaptic vesicle and the plasma membrane, as well as cytoplasmic proteins. Some of these proteins, e.g., synapsin alphaSNAP, and Ca2+ channels are known to be the downstream targets of PKA. Phosphorylation of these proteins may be important for the regulation of vesicle mobilization, docking, and fusion (Yao, 2000).

In Drosophila dnc mutants, increased cAMP levels caused by the disruption of a phosphodiesterase lead to abnormalities in channel function and nerve excitability, synaptic transmission and plasticity, growth cone motility, and nerve arborization. Using the present heterologous detection system, the altered transmitter release process could be examined in developing growth cones of dnc central neurons in isolation from the influence of postsynaptic targets. Examination of PKA-RI neurons suggests that the dnc defects in ACh secretion might be mediated by PKA. These results establish a role for the cAMP cascade in the regulation of the secretion process in developing neurons before synaptogenesis. In light of the profound alterations in synaptic efficacy and activity-dependent modulation observed in mature synapses of dnc mutants, the cAMP pathway may be involved throughout the maturation process of the synapse (Yao, 2000).

The effects of decreased cAMP levels on synaptic transmission have also been extensively studied in Drosophila. Intracellular recordings at the peripheral larval neuromuscular junction have revealed that chronically lowering cAMP causes reduced neurotransmitter release, likely because of reduction of innervation rather than impairment of transmitter release. These results do not contradict results obtained from developing central neurons. It will be important to determine how reduction in cAMP concentration affects neurotransmitter releases in the Drosophila central neurons in future studies (Yao, 2000).

The prolonged ACh currents of dnc and PKA-RI neurons may be attributable to increased ACh diffusion distance and altered presynaptic release mechanisms, as discussed above. A reduced efficiency in the formation of the exocytotic fusion pore and/or a disrupted fusion machinery may account for the prolonged release events for synaptic vesicles containing similar amounts of ACh. Exocytotic efficiency may be regulated by PKA-dependent phosphorylation of vesicular, cytoplasmic, and plasma membrane proteins involved in exocytosis. Additional mutational analysis will be required to identify the specific proteins that are targeted by PKA in this process (Yao, 2000).

Although the spontaneous release in neurons of all genotypes examined does not require Ca2+ influx, the activity-dependent increase in release frequency in dnc neurons after repetitive nerve stimulation appears to depend on the external Ca2+. It has been proposed that nerve activity regulates cAMP levels, possibly mediated by intracellular accumulation of Ca2+ through repetitive nerve spikes, which can trigger the Ca2+/CaM activation of adenylyl cyclase. The activity-dependent modification of transmission at mature synapses is altered in dnc mutants. These results suggest that the cAMP pathway may mediate such activity-dependent regulation in developing neurons before synaptogenesis as well, lending support to the notion that the cAMP pathway is important in a wide variety of neuronal processes throughout development (Yao, 2000).

Cyclic adenosine monophosphate metabolism in synaptic growth, strength, and precision: neural and behavioral phenotype-specific counterbalancing effects between dnc phosphodiesterase and rut adenylyl cyclase mutations

Two classic learning mutants in Drosophila, rutabaga (rut) and dunce (dnc), are defective in cyclic adenosine monophosphate (cAMP) synthesis and degradation, respectively, exhibiting a variety of neuronal and behavioral defects. This study asked how the opposing effects of these mutations on cAMP levels modify subsets of phenotypes, and whether any specific phenotypes could be ameliorated by biochemical counter balancing effects in dnc rut double mutants. This study at larval neuromuscular junctions (NMJs) demonstrates that dnc mutations caused severe defects in nerve terminal morphology, characterized by unusually large synaptic boutons and aberrant innervation patterns. Interestingly, a counterbalancing effect led to rescue of the aberrant innervation patterns but the enlarged boutons in dnc rut double mutant remained as extreme as those in dnc. In contrast to dnc, rut mutations strongly affect synaptic transmission. Focal loose-patch recording data accumulated over 4 years suggest that synaptic currents in rut boutons were characterized by unusually large temporal dispersion and a seasonal variation in the amount of transmitter release, with diminished synaptic currents in summer months. Experiments with different rearing temperatures revealed that high temperature (29-30°C) decreased synaptic transmission in rut, but did not alter dnc and wild-type (WT). Importantly, the large temporal dispersion and abnormal temperature dependence of synaptic transmission, characteristic of rut, still persisted in dnc rut double mutants. To interpret these results in a proper perspective, previously documented differential effects of dnc and rut mutations and their genetic interactions in double mutants on a variety of physiological and behavioral phenotypes were reviewed. The cases of rescue in double mutants are associated with gradual developmental and maintenance processes whereas many behavioral and physiological manifestations on faster time scales could not be rescued. Factors that could contribute to the effectiveness of counterbalancing interactions between dnc and rut mutations for phenotypic rescue are discussed (Ueda, 2012).

It has been demonstrated that cAMP levels are decreased in rut. The results clearly contrast the differential effects of disruptions in synthesis and degradation of cAMP on synaptic function and nerve terminal morphology. Mutations in dnc, including dnc1, dncM11, and dncM14, can lead to severe defects in nerve terminal branching and bouton morphology. Aside from this study, previous reports have documented in identified larval muscles that total bouton numbers and motor terminal branching pattern are severely affected by dnc, but these defects were not detected in rut. A similar situation has been reported in the adult CNS: axon terminal growth in the mushroom body is enhanced in dnc but is not affected in rut. In contrast, rut and dnc mutations both have clear effects on synaptic transmission but in distinct manners. Increased cAMP levels in dnc could enhance transmitter release (as indicated by increased ejp sizes with a minimal disturbance in the temporal precision of the release process. In comparison, rut mutations more severely disrupt temporal control of release, regardless of the rearing temperature. In addition, the rearing temperature affects the amplitude of synaptic transmission in rut, with strongly depressed transmission at high temperature. This likely reflects a decrease in vesicle release because the miniature ejp size was unaltered at different temperatures (data not shown) (Ueda, 2012).

A number of mutant alleles of the rut gene have been described in the literature of developmental studies, but the alleles frequently used in neurogenetic experiments are limited to rut1, rut2, rut3, rut1084, and rut2080. Furthermore, only three mutant alleles have been biochemically characterized in Drosophila: rut1, rut2, and rut3. It should be mentioned that these rut mutations can cause significant decrease in total cAMP synthesis despite the fact that there are at least four adenylyl cyclase (AC) homologous genes that have been identified molecularly and biochemically in Drosophila. This raises the possibility that rut may represent a major AC gene but all AC genes may play differential roles in regulating cAMP levels, depending on their subcellular localization and conditions to activate their actions. As demonstrated in this study as well as in earlier reports, a general pattern of relative severity among several rut mutant alleles is observed across different phenotypes, as represented in the following sequence: rut1 = rut1084 = rut2 = rut3 = WT (Ueda, 2012).

Compared to the AC genes, there appears to be fewer PDE homologous genes and only two genes are known for their cAMP degradation action besides dnc. However, dnc gene products are represented by more than 10 splicing variants as opposed to 2 rut splicing variants. There are a large number of dnc mutant alleles reported in literature but only a small number of them are frequently used in neurogenetic studies, i.e., dnc1, dnc2, dncM11, and dncM14. Interestingly, a consistent pattern of phenotypic severity can be observed across different phenotypes among these four alleles: dncM11 = dncM14 = dnc1 = dnc2 (Ueda, 2012).

A comparison of their effects on a variety of phenotypes includes PDE enzyme activity disruption, defective growth cone motility of cultured neurons, enhanced growth of larval NMJ, enhanced K + and Ca2 + currents in larval muscles, decrease in the larval motor neuron firing frequency upon depolarization, increase in whole-cell ejps or ejcs, and decrease in activity-dependent facilitation of synaptic transmission at larval NMJ, decrease in the habituation rate of olfactory jump response and odor-electric shock association in adult flies, and female sterility. In a different approach, overexpression of a UAS-dnc + transgene in motor neurons results in reduced NMJ growth and decreased ejp size even in larvae reared at room temperature. These phenotypes demonstrated the effects of increased cAMP degradation in contrast to those caused by dnc mutations (Ueda, 2012).

When considering their mechanisms of action, several reported phenotypic effects of dnc alleles may be complicated by the implications of contributions from the genetic background. Notably, the dncM11 mutant line has been reported to affect protein kinase C (PKC) activity in addition to PDE. In addition, the severity of dnc1 may in fact be more extreme than reported, since dnc1 has been shown to be female sterile once a second-site mutation near the dnc locus is removed from the original fertile line. It is possible that many dnc1 lines used in neurogenetic investigations contain this mutation in the background (Ueda, 2012).

A number of experimental paradigms have been used to characterize behavioral and physiological phenotypes of dnc and rut mutants with defined quantitative parameters. For a majority of phenotypes examined, dnc and rut mutations do not lead to opposite effects on these quantitative indices, even though they alter the cAMP levels in opposite directions. Only for certain phenotypes, the dnc and rut mutations affect the parameters in opposite directions. For example, in larval neuromuscular synaptic boutons, mobilization of synaptic vesicles from the reserve pool to exo/endo cycling pool is suppressed in rut and enhanced in dnc. Similarly, the number of docked vesicles at synapses is decreased in rut and increased in dnc. Ca2 + current measured in larval muscles is decreased in rut and increased in dnc. Hyperexcitability-induced overgrowth of larval NMJ can be suppressed by rut but enhanced by dnc. Similarly, dnc and rut mutations exert opposite effects on Kenyon cell axon counts in the mushroom body of developing adult flies. Finally, habituation rate of the giant fiber escape circuit is decreased by rut and increased by dnc (Ueda, 2012).

In contrast, for some other phenotypes, rut alleles have no apparent effects while dnc mutants display clear alterations. For instance, the larval NMJ terminal projection pattern and adult mushroom body axonal terminal growth were altered in dnc but not in rut. Moreover, identified K + currents in larval muscles are increased in dnc but unaltered in rut. In these cases, increased cAMP levels can produce abnormalities but underlying mechanisms may be tolerant to depleted cAMP levels (Ueda, 2012).

For another group of phenotypes, dnc and rut mutations can affect separate parameters and sometimes produce superficially similar effects by altering a parameter in the same direction. Such cases include decreased growth cone motility, irregular action potential firing pattern, and modified intracellular Ca2 + dynamics in cultured neurons. In larval neuromuscular junctions, both dnc and rut decrease synchronicity of synaptic transmitter release and presynaptic facilitation of neuromuscular transmission. During post-eclosion development of adult flies, both dnc and rut mutations enhance the axon terminal growth of mechanosensory cells and decrease the structural and functional adaptation of the olfactory system to odor exposure. Neither dnc nor rut mutants respond to environmental or social deprivation in modifying Kenyon cell axon counts of young adults. Mutations of either dnc or rut decreases habituation rate of the proboscis extension reflex and olfactory avoidance and jump response, and the performance indices of both classical and operant conditioning. Studies on alcohol response have demonstrated increased sensitivity in rut alleles but no apparent change in dnc alleles. Although it is reassuring to observe opposite effects of dnc and rut mutations on some of the quantitative parameters, it should be noted that it is not straightforward in associating most of the indicators with the defective mechanisms directly regulated by cAMP signaling. Dysfunction in AC and PDE may exert opposite effects on some cell biological mechanisms or neural circuit components but can still lead to apparently similar deficiencies of a cellular function or behavioral task (Ueda, 2012).

Some insights may be gained through examining the genetic interactions between dnc and rut in double mutants about how rut AC and dnc PDE are involved in particular aspects of physiological or behavioral plasticity. At the present time, only a limited number of reports document the resultant phenotypes in dnc rut double mutants. Significantly, the majority of the single-mutant phenotypes of dnc or rut mutations do not become less severe in dnc rut double mutants, even though the overall cAMP levels are largely restored. The phenotypes that are not rescued in double mutants include increased bouton size in dnc and impaired synchronicity of transmitter release in larval NMJs, irregular firing of cultured neurons, and habituation and olfactory associative learning of adult flies (Ueda, 2012).

However, a few cases of successful rescue in double mutants have been described. Decreased growth cone motility in dnc and rut neurons in culture can be restored by combining two mutations and the overgrowth and altered projection patterns of dnc larval motor terminals is suppressed in dnc rut. Interestingly, none of the above cases of successful rescue involve opposite effects of dnc and rut single-mutant phenotypes. Notably, both cases of restoration involve a particular allele, rut1. The allele rut1 is different from other alleles with characterized AC enzyme activity (rut2 and rut3) in that the Ca2 + /CaM-dependent activation of AC is eliminated in rut1 flies, but retained in rut2 and rut3. Unlike rut1, the allele rut2 is not able to rescue the dnc mutational effects of enhanced larval NMJ growth and irregular firing in cultured neurons. In the present study of NMJ focal recording, it was clears that rut2 did not affect the precision in release timing (ejc peak time) and ejc amplitudes, although rut1 decreased the temporal precision of release (increased variability in ejc peak time) and the ejc amplitude significantly. It will be helpful if further experiments are performed on additional allele combinations of dnc and rut to delineate the role of Ca2 + -dependent regulation of AC in specific phenotypes of interest (Ueda, 2012).

In addition to peculiarities of enzymatic properties in mutant alleles, e.g., rut1 AC devoid of Ca2 + /calmodulin (CaM) sensitivity, other factors influencing interactions between dnc and rut must be considered. As summarized above, counterbalancing rescue of dnc and rut phenotypes in double mutants is likely to be exceptions rather than a general rule. Therefore, it would be desirable to identify the conditions and factors that could facilitate their counterbalancing interactions, which may provide insights into the orchestration of dnc PDE and rut AC underlying the phenotype of interest (Ueda, 2012).

First, it is important to consider the temporal and spatial characteristics of expression and operation of these enzymes. In the temporal domain, their effects on a variety of phenotypes are mediated through integration among different biochemical pathways and cellular processes, some of which may function with rapid kinetics, whereas others may represents slow accumulation of products through a number of steps. Some of the resultant phenotypes may require continuous adjustment in response to internal or environmental conditions while others may appear relatively permanent and irreversible, possibly associated with developmental events (Ueda, 2012).

The spatial factors to be considered include the cellular expression and subcellular localization of the enzymes. To the best of our knowledge, there is little information about whether dnc PDE and rut AC are colocalized in molecular assemblies or aggregates within certain functional domains in specific neuronal cell types. Close proximity of AC and PDE localization facilitates local regulation of cAMP levels within a short time. Certain cellular processes with slower kinetic steps also facilitate integration of dnc and rut interactions, extending their balancing acts to a broader spatial range (Ueda, 2012).

For the few examples of successful counterbalancing rescue, growth cone motility seems to be a continuous adjustment by cAMP on a time scale of tens of seconds to minutes. This relatively slow kinetics makes it possible to readily manipulate the cAMP signaling pathway, e.g., bath application of db-cAMP increases rut growth cones motility, mimicking dnc counter balancing effects in double-mutant growth cones. Some developmental or maintenance processes, such as axonal path finding, branch formation, target interaction, and synaptogenesis, are also slow adjustment processes (in the order of hours to days). In these cases, restoration of cAMP levels through long-range interactions of AC and PDE may be sufficient to rescue the single-mutant phenotype. For example, dnc defects in larval motor terminal growth are suppressed by rut1 (Ueda, 2012).

In contrast, defects in some physiological properties (K + currents, neuronal firing, and transmitter release timing) and behavioral conditioning (habituation and classical conditioning) cannot be rescued by combining dnc and rut, which sometimes leads to even more extreme deficiencies, e.g., the extremely rapid habituation in dnc rut. One possibility is the requirement of dynamic cAMP regulation within a short time period (millisecond to second range) during which a counterbalancing act is difficult to achieve. Another possible explanation is the requirement of unimpaired cellular machinery laid down during development (e.g., proper channel and receptor localization) and functional connectivity among synaptic partners (inhibitory and excitatory elements in the circuit) underlying behavioral phenotypes under consideration. Deviation from coordinated actions of such subcellular machinery or circuit components will make it difficult to obtain compensatory rescue (Ueda, 2012).

It should be noted that well-defined abnormalities in central fiber projection have been reported in dnc and rut single mutants that reflect the alterations in peripheral motor terminals in larval NMJs. Furthermore, dnc PDE and rut AC are preferentially expressed in mushroom bodies, which are important in odor-associated learning. Therefore, it is reasonable to speculate that defects in higher functions, including classical associative learning and habituation, may involve anatomical defects in the CNS, such as altered dendritic arbors and synaptic connections detectable in certain defined circuits, in addition to potential changes in synaptic physiology (Ueda, 2012).

Cell-specific expression and subcellular localization of AC and PDE isoforms may affect dnc and rut single-mutant, as well as double-mutant phenotypes. These include splicing variants of the dnc and rut gene as well as the products of their homologous genes. Such complexity needs to be considered in the interpretation of dnc and rut interactions in order to appreciate contributions of individual splicing variants and to delineate influence from their homologous genes (Ueda, 2012).

Finally, cross-talk between the cAMP and other signaling pathways can also modify dnc and rut phenotypes. For example, variety of signalling pathways are known to converge onto the CREB transcription factor. It is also established that not only the cAMP cascade but also other signaling pathways, including PKG and CaMKII, can modify larval NMJ physiology and morphology as well as adult habituation, courtship conditioning and classical conditioning. It will be of particular interest to establish the consequences of such genetic interactions across signaling pathways. Double mutant analysis in conjunction with transgenic and genomic approaches remains a powerful and profitable direction for revealing the genetic network underlying neural and behavioral plasticity (Ueda, 2012).


The complexity of the dunce locus and its transcription products points to the biological importance of Dunce. The dunce gene encodes multiple RNAs ranging in size from 4.2 to 9.6 kb (1 kb = 10(3) bases). Six different classes have been identified. Exons are distributed over more than 148 kb of genomic DNA, with some exons being used alternatively among the RNAs. The RNAs are transcribed from at least three initiation sites. Some of the heterogeneity is generated by using varying lengths of a 3'-untranslated trailer sequence. The protein variation potentially includes N-terminal differences coded for by transcript-specific 5' exons, internal differences arising from the optional inclusion of a 39 base-pair exon, and the alternative use of two 3' splice sites separated by six base-pairs. An unusual feature of the dunce gene is the presence of at least 7 other genes nested between the dunce exons. The significance of this phenomenon is unknown (Qui, 1991 and Nighorn, 1994).


Amino Acids - 702, 714 and 777 for three isoforms (Qui, 1991).

Structural Domains

The deduced amino acid sequence is strikingly homologous to the amino acid sequence of a Ca2+/calmodulin-dependent cyclic nucleotide phosphodiesterase isolated from bovine brain and more weakly related to the predicted amino acid sequence of a yeast cAMP phosphodiesterase. These homologies, together with prior genetic and biochemical studies, provide unambiguous evidence that dunce+ codes for a phosphodiesterase. In addition, the dunce+ gene product shares a seven-amino acid sequence with a regulatory subunit of cAMP-dependent protein kinase that is predicted to be part of the cAMP binding site. There is also a weak homology between a region of the dunce+ gene product and the egg-laying hormone precursor of Aplysia californica (Chen, 1989).

dunce: Evolutionary Homologs | Regulation | Developmental Biology | Effects of Mutation | References

date revised: 29 June 2000 

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