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Don't have an account? This seems unlikely since in the presence of light, the controls do not show a reduction in sleep. The fact that the flies sleep more in constant light than in constant dark also seems extremely unusual. Teng et al. Furthermore, do Nca protein levels vary between sleep-wake states to explain why it is only important during sleep? Rat and likely other mammalian Hippocalcin antibodies are commercially available, given that the Teng et al.

The previous manuscript suggested it was dopamine receptors, now the Discussion mentions NMDA receptor internalization. Thank you for resubmitting your work entitled "Neurocalcin regulates nighttime sleep and arousal in Drosophila " for further consideration at eLife. The manuscript has been improved but there are some remaining issues that need to be addressed before acceptance, as outlined below.

Please address these to the best of your ability. This should have asked what combinations of Gal4 drivers the authors did test, since this kind of negative data is useful for interpreting how exclusive the network of neurons involved is. As it stands, the reason why the C01 and A05 Gal4 drivers were chosen as the specific combinations seems a little odd.

Under what light conditions were those flies entrained? It would be useful to also show the activity patterns under LD conditions, preceding release into DD. First with TrpA1 activation. Second with dORK silencing. I find the first experiment reasonable, but the second experiment much less compelling. However, constitutive dORK expression is known to irreversibly damage neurons. As I understand it, either outcome could produce the observed result.

This conclusion is based on spatially limiting the RNAi effects, thus defining brain regions that are necessary. It does not preclude involvement of other regions.

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Therefore this conclusion over-interprets the data. In supplement 6, CG appears to be distinct and non-overlapping. Which is true? The manuscript has been improved but there are still some remaining issues that need to be addressed with before acceptance. Please make textual changes according to the suggestions of the reviewer as outlined below:. The authors have addressed all the points raised in the last round of review. For the most part, I feel the responses were appropriate.

In some cases, I have continued questions. Interpretation of dORK effects - The authors make a forceful argument against the possibility of prolonged dORK mis-expression causing irreversible developmental effects. They suggest that the lethality observed with driving hid or reaper transgenes contrasts with the viability of driving dORK and hence the neurons must be "healthy". I disagree because such lethality may well result from damage to non-neuronal tissues: the fly-light lines are described for their neural expression patterns, but non-neuronal expression is not generally described or precluded.

Hence this result does not bear on the question of neuronal health following prolonged dORK expression. Likewise, it is not clear why locomotor activity levels in flies would necessarily be affected if C01 - and A05 neurons were partially damaged. The use of UAS-shi[ts] in the Nca knockdown background is more compelling because it is a conditional design and because it provides a result in line with the hypothesis. However, it is not included in the paper for technical reasons so it cannot stand as a "complete" result, and likewise it cannot serve as a sub-textual proxy to justify inclusion and interpretation of the prolonged dORK expression experiment.

I was wrong in stating the literature documents irreversible damage to Drosophila neurons with prolonged dORK expression and so I agree with the authors in their statement to that regard. However, the literature is clear in documenting the irreversible damage to Drosophila neurons with prolonged Kir expression, which as shown by White and colleagues, works in comparable fashion to dORK by imposing a hyperpolarized state. I suggest the important issue is whether prolonged hyperpolarization of Drosophila neurons is beyond reasonable doubt an effective means to exclusively affect neurotransmission.

Ceriani and colleagues in showed that prolonged expression of Kir in LNv pacemaker neurons irreversibly affected molecular oscillations, structural maturation and neuropeptide content. In contrast, restricting Kir expression to adult stages, led to outcomes that were at least partially reversible. Therefore, I hold to the opinion that the present dORK experiment is not compelling, in spite of the additional observations provided. If the authors insist on its inclusion, then I think it's important to share with readers a clear caveat based on the Ceriani work. I think it would be useful to make this point clear in the text - for example on line of the revision, CG is described as a "neighboring" locus.

I interpret "neighbor" as independent or free-standing. These two genes are overlapping or in some fashion "compound". I recommend the text include a clear description of this genomic arrangement and be re-examined to ensure clarity on this point in all mentions. Likewise, I suggest inclusion of the RNAi knockdown results of CG as supplemental information to allay concerns on this point.


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Regarding that experiment, one other minor point: in the response and author response images, the authors describe using two different RNAi's from NIG. The figure leads the reader to think two different RNAis were tested. We sincerely thank the reviewers for their insightful comments relating to our manuscript.

Collectively, these have prompted us to strengthen the focus of the paper more appropriately towards the role of Neurocalcin as a novel sleep gene in Drosophila. As noted by reviewer 1, current data suggest that Hippocalcin mutations are rare amongst dystonia patients. Nonetheless, the potential genetic links between human dystonia and Drosophila sleep were in fact highly relevant to how we initially identified Neurocalcin as a sleep gene.

For brevity, we initially omitted the actual screening strategy that led us to focus on Neurocalcin , but we now describe this in more detail in our Introduction as we believe this approach will be of interest to the community. Importantly, our revised manuscript not only addresses the reviewer concerns detailed below but also contains abundant new mechanistic data regarding how Neurocalcin solely promotes night sleep.

Firstly, in our revised Figure 2, we combine video tracking with mechanical stimulation to probe daytime versus night time arousal in Neurocalcin knockdown, knockout and respective control flies. We find that knockdown or knockout of Neurocalcin does not impact the probability of response to a mechanical stimulus during the day Figure 2A-B, E , but significantly lowers the arousal threshold during the night Figure 2C-D, F. Arousal thresholds are known to dynamically vary over 24 h in Drosophila , with day sleep having a lower arousal threshold than night sleep Faville et al.

Our identification of Neurocalcin as a specific regulator of night time arousal will therefore be of substantial interest to the sleep field. Secondly, we have investigated how this night-specific effect is gated. We show in our revised Figure 3 that both the circadian clock and light are capable of gating when Neurocalcin promotes sleep, likely via inhibiting the wake-promoting effect of loss of Neurocalcin during the day.

We also present data showing that the CRY blue-light photoreceptor is involved in this process. Collectively, these new data combined with alterations to the manuscript significantly enhance both our mechanistic understanding of how Neurocalcin impacts night sleep and the overall robustness of our work. Below, we further respond to each individual reviewer comment. We fully agree with the reviewer. Instead, the most important finding wrt to dystonia is the genetic interaction between Nca and the dopamine receptor.

We performed a series of experiments to address this important question. However, before describing these, it is relevant to give a brief overview of the particular mutant lines used to examine epistatic interactions between Neurocalcin and Dop1R1. In our initial experiments we used two transposon insertions in the Dop1R1 locus on chromosome III of Drosophila as independent alleles that were likely loss-of-function. Due to the known importance of genetic background on sleep in Drosophila Cirelli et al. However, we could not outcross chromosome III itself while easily following the Dop1R1 alleles themselves, as there was no visible marker within the transposons that could be observed in the iso31 background.

To both better control for genetic background and achieve cell-specific Dop1R1 knockdown, we therefore used two complementary approaches. Firstly, we outcrossed a transgenic RNAi line targeting Dop1R1 for 5 generations into the iso31 background. Secondly, we outcrossed a previously characterised hypomorphic allele of Dop1R1 called dumb 2 Kim et al. However, in contrast to our previous results where heterozygosity for either Dop1R1 allele rescued sleep loss in Neurocalcin knockdown flies, neither expression of outcrossed Dop1R1 RNAi, nor homozygosity for the outcrossed dumb 2 allele, suppressed the effect of pan-neuronal Neurocalcin knockdown Author response image 1A-D ; original results are shown in Author response image 1E-F for reference.

Mean sleep levels are shown in A across 24 h in L8: D16 conditions, while median night sleep levels are shown in B. C-D Night sleep levels in Nca KO red lines flies are reduced as compared to iso31 controls grey line. However, this sleep loss is not suppressed by homozygosity for the hypomorphic dumb 2 allele of Dop1R1 purple line. Mean sleep patterns were shown in the original Figure 2G.

Median total night sleep levels were shown in the original Figure 2H.

Summary Bibliography: Catherine Mintz

Control and experimental genotypes are indicated by color scheme and black dots. Given these conflicting results, which we assume are due to differences in genetic background between the fully and partially outcrossed Dop1R1 alleles and RNAi insertions, we have removed Figure 2G, H from the manuscript. Several independent lines of evidence argue for a role for Neurocalcin in regulating sleep rather than an independent physiological variable that could cause nighttime hyperactivity.

Secondly, the fact that sleep loss in Neurocalcin knockdown flies only occurs in the subjective night of constant dark conditions new data presented in Figure 3A in our revised manuscript shows that loss of Neurocalcin does not simply cause hyperactivity in the absence of light. Instead, sleep loss is clearly regulated by the circadian clock.

This again supports a direct sleep-regulatory role of Neurocalcin , since sleep onset is gated by the circadian clock Borbely, Finally, the clear and sustained startle-responses to lights-off in Neurocalcin knockout males Figure 1N, O of revised manuscript also strongly suggests that these mutants are able to detect the absence of light. We cannot fully rule out the possibility that Neurocalcin regulates hunger specifically during the night, but this hunger would have to be gated by the clock and light in such a way that it was suppressed during constant light conditions, as we observe no sleep loss in Neurocalcin knockdown flies under this condition see Figure 3G, H in revised text.

We consider it far more likely that Neurocalcin is indeed a bona fide sleep-promoting gene. To address this point we have now measured sleep levels in three additional combinations of Nca knockout alleles Figure 1—figure supplement 6. Thus, in total we have shown using four combinations of Nca knockout alleles and three independent Nca RNAi lines that reducing NCA expression consistently results in night-specific sleep loss.

Collectively, these results robustly support a role for NCA in regulating night sleep. To clarify, in our mini-screen of individual neuronal subpopulations, there was no subset in which Neurocalcin knockdown resulted in night sleep loss, including C5 Gal4 and two other FSB-positive driver lines see Figure 4—figure supplement 1 of revised manuscript. We believe the colour scheme in our original figure may have been slightly confusing, so we have changed the colour-coding and the text within the figure accordingly to emphasise that only Neurocalcin RNAi driven by elav -, nsyb - and inc -Gal4 yielded significant sleep loss relative to both driver and transgene alone controls.

This is consistent with many studies of sleep genes in Drosophila , including sleepless , insomniac , taranis and cyclin-A , all of which failed to identify a single neuropil region that fully accounted for sleep loss in these mutants. We note that previously studied sleep regions such as the fan-shaped body Donlea et al.

Identifying these subdomains will be a fruitful avenue of future investigation.

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We agree with the reviewer that this is an interesting question. Nonetheless, since we observed no clear difference between our own images of C01 - and A05 -Gal4 expression within the MB region Figure 4A, C and those acquired by the Janelia Flylight team Jenett et al. Finally, despite lacking their characteristic tiling pattern Aso et al. For comparisons of effect sizes, the reduction in night sleep caused by Nca knockdown in A05 - and C01 -neurons is shown in Author response image 2E.

We have set out to further examine this hypothesis as a separate follow-up project by using A05 -Gal4 in parallel with an array of defined MBON split-Gal4 drivers. These manipulations did not result in night sleep loss Author response image 2F. Images are from Jenett et al. Images were downloaded and digitally superimposed Merged onto a standardised fly brain active zones are labelled in blue using the nc82 antibody; the image source data is distributed under a CC BY-NC-SA 4.

E Nca knockdown in both A05 - and C01 -positive neurons results in robust night sleep loss. For C-E , please see Figure 5—figure supplement 2G for nvalues. Nonetheless, it is important to note that the contribution of these neurons is modest. While these results have provided us with potential insights into the contribution of subsets of MBONs to sleep loss in Nca knockdown flies, a comprehensive Nca knockdown screen with higher resolution within KCs and MBONs without involving A05 - and C01 -Gal4 will be required in the long term.

Moreover, we interpret this data with caution because the MBON split-Gal4 driver lines have not been outcrossed into the iso31 background. Since the effect of Nca knockdown on sleep appears to be susceptible to modification by genetic background Author response image 1 , we will solely include data from the outcrossed A05 -, C01 -, and ok -Gal4 lines in our manuscript, and follow up these studies once the individual components of the MBON split-Gal4 lines are fully outcrossed and subsequently recombined.

We concur with the reviewer. We have instead emphasised that Neurocalcin is required in a dispersed network consisting of multiple neuropil domains see Discussion, second paragraph. This conclusion is more strongly supported by our Neurocalcin knockdown data presented in Figure 4 and associated figure supplements We attempted to perform cell-specific knockdown experiments to examine this interesting question. However, as described above and in Author response image 1 , due to inconsistencies between different Dop1R1 alleles and RNAi lines likely due to differences in genetic background we have decided to remove the data shown originally in Figure 2 describing a genetic interaction between Neurocalcin and Dop1R1.

To compensate, we now add substantial mechanistic data revealing a specific role for Neurocalcin in regulating arousal during the night but not the day, and illustrating a dual role for circadian and light-sensing pathways in gating the timing of this effect presented as Figures 2 and 3 in revised text.

We attempted to address this point. Surprisingly, expression of this transgene failed to rescue Nca knockout flies. We therefore made V5-tagged or untagged UAS- Nca transgenes in-house and generated a second set of stable transgenic fly lines. These also failed to rescue the Nca knockout or knockdown phenotypes when expressed in neurons using the elav -Gal4 driver. We believe we now understand the reason for this lack of rescue. A negative control for leaky transgene expression transgene insertion alone in the absence of the C01 driver is shown in C. This staining was specific as an anti-V5 antibody alone did not label any neuropil region Author response image 7C.

Clearly, there is an unknown element lacking in our transgene sequence that is limiting Neurocalcin protein expression, which we are now attempting to identify. Unfortunately, these complications have precluded addition of rescue data in our current manuscript. Nonetheless, it is important to note that four combinations of independent Neurocalcin knockout alleles see Figure 1—figure supplement 6 and three independent RNAi lines all yield consistent night-specific sleep phenotypes.

Thus, the link between Neurocalcin and night sleep is genetically robust. As noted above, we have rewritten the manuscript to focus on the sleep-regulatory role of Neurocalcin. Therefore, we have removed the locomotor activity plots previously described in Figure 1—figure supplements 2 and 4 in order to focus more appropriately on the sleep phenotype of Neurocalcin knockout and knockdown flies.

Using video-tracking velocity data from the DART system, we previously provided waking velocity data during the evening activity peak and the normally quiescent period during the night. We have also now included average velocity data across the entire 24 h period, showing reduced overall wake velocity in Nca KO flies. These data are included in Figure 1—figure supplement 8A-D of the revised text. One such experiment would be to manipulate the A05, C01, and OK knockdowns of neurocalcin and relevant combinations in the arousal assay, in DD, and in LL, similar to what was done in Figure 2 and Figure 3A and G for the pan-neuronal knockdown, and possibly combining the LL treatment with some of the functional imaging presented in Figure 5.

We thank the reviewers for these excellent suggestions. We also examined whether the nighttime arousal threshold was altered by Nca knockdown in C01 - and A05 - neurons. This was indeed the case, while daytime arousal was unaffected Figure 4G-H. Thus, Nca knockdown in C01 - and A05 - neurons phenocopies the nighttime sleep loss and increased arousal observed in Nca mutants or following pan-neuronal Nca knockdown.

G-H Median subjective night sleep G or total sleep H for the above genotypes in either constant-dark G or constant light H. However, while these results are intriguing and will certainly form a platform for further interesting experiments, we feel that these data will likely confuse the readers of our paper, as we do not currently possess a robust understanding of how clock and light-sensing pathways differentially interact with each sub-circuit under LL or DD conditions.

Our manuscript will thus focus on simultaneous Nca knockdown in C01 - and A05 -neurons or in one section, ok - and A05 -neurons in either 8L: 16D or LL. We found that Nca knockdown in either C01 - or ok -neurons significantly enhanced arousal during the night, resulting in the nighttime arousal threshold becoming more similar to the daytime arousal threshold Figure 6A-D.

Relative to controls, we found no significant difference in arousal following Nca knockdown in A05 -neurons during the day or night Author response image 5E-F. The reviewers also requested us to examine how LL conditions impact neural excitability in C01 - and A05 -neurons following Nca knockdown. Since Nca knockdown in C01 - and A05 - neurons causes robust night sleep loss in 8L: 16D and DD but not in LL, we hypothesized that constant light might suppress this enhanced synaptic output. This was indeed the case Figure 7E-H. We examined the above questions by knocking down Nca expression via transgenic RNAi in cry -positive neurons alone using the most widely expressed cry -Gal4 cry -Gal; Zao et al.

However, given that the circuit logic of this effect remains unclear, we have not included these data in our manuscript. We agree that light is unlikely to inhibit NCA function directly. To address the reviewers concern about constant light increasing sleep levels compared to constant dark, we first examined whether this could be due to a genetic background effect. We measured sleep levels in isogenic iso31 flies our control stock or in non-isogenic Canton-S male flies.

In both cases, total sleep levels were significantly increased in LL compared to DD Author response image 7. Thus, in our recording conditions, constant light enhances sleep. Median total sleep across 24 h in either constant-dark DD or constant-light LL are shown for adult males from four different genetic backgrounds. While sleep levels in LL, LD and DD are rarely compared in the literature, other manuscripts support our observations. For example, in work performed by the Koh lab Afonso et al. Other groups have also investigated sleep levels in constant light, for example, the Griffith lab Parisky et al.

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The baseline sleep levels under LL in these works do appear to be lower than our own. However, in both cases females rather than males were studied under LL. Given that male flies exhibit more daytime sleep compared to females i. We agree that the NCA immuno-staining published in Teng et al. We undertook several independent approaches to attempt to fill this knowledge gap. However, using these custom antibodies we were unable to detect NCA protein in the fly brain by western blot or immuno-staining. Since the antibody generated by Teng et al. However, we were unable to obtain this antibody.

Unfortunately, we did not detect NCA-specific signals in the fly brain with this antibody. We are in the process of generating knock-in flies with V5-tagged NCA under the control of the endogenous Nca promoter, which will enable the cellular and sub-cellular expression of NCA to be defined in detail. However, due to time constraints we are unable to add this data to the manuscript.

However the same NMADR1 mutation also caused significant sleep loss in the presence of the elav -Gal4 insertion Author response image 8 , blue asterisks. Hence, the enhancement of sleep loss in Nca knockdown flies appears to be additive. In our Discussion, we have clarified the text to make clear that NCA may be acting through multiple molecular pathways potentially involving post-synaptic receptors and presynaptic ion channels to regulate neurotransmitter release, similarly to its mammalian homologue Hippocalcin. B Median night sleep levels in the above genotypes.

We agree with the reviewers that the assignment of A05 - and C01 -neurons as either pro-arousal or modulatory is over-simplified. In 8L: 16D, thermogenetic excitation of these neurons using TrpA1 Figure 8 suggests that C01 -neurons are strongly wake-promoting, whereas activation of A05 -neurons only promotes wakefulness in the context of parallel C01 -neuron activation.

We thank the reviewer for highlighting this error, which we have now corrected. We have added negative data from eight additional combinations of driver lines to Figure 4—figure supplement 1B. Secondly, since light-sensing pathways modulates the wakefulness in Nca knockdown flies, we investigated two circuits that transmit light information: tubercular-bulbar neurons, subsets of which we and others have demonstrated are sleep promoting Lamaze et al.

Tubercular-bulbar neurons are labelled by the A05 -Gal4 driver and additional drivers shown in Figure 4—figure supplement 1B. We have modified Figure 1—figure supplement 5 to more clearly show the first day in LD preceding release into DD, and have included details of how these flies were entrained in the Materials and methods section. Briefly, flies were entrained in 12L: 12D cycles for three days before transfer to DAM tubes, after which fly activity was recorded for one day in 12L: 12D before release to DD.

For example, Nitabach et al. Similarly, Kremer et al. Firstly, as a positive control to assess the impact of damaging C01 - and A05 - neurons, we expressed the pro-apoptotic genes hid and reaper in either C01 - or A05 -neurons alone. However, if this phenotype was solely due to a non-specific decline in neuronal health rather than an inhibition of synaptic release, we would expect acute silencing of C01 - and A05 -neurons to have no impact on sleep levels following Nca knockdown. Therefore, we have not included this data in the manuscript. Driver and transgene alone controls are also shown.

B Box plots comparing median peak activity at ZT8 the evening activity peak. We have modified this figure to remove any irrelevant non-transcribed regions from each of the Nca and cg isoforms shown in Figure 1—figure supplement 2A. We also modified the corresponding figure legend to emphasise that transcript isoforms are shown in this figure supplement. In Figure 1—figure supplement 6A we depict the genomic region and surrounding sequences corresponding to the targeting arms used for homologous recombination. As shown in Author response image 10 , in contrast to Nca knockdown, neither RNAi line targeting cg altered total night sleep levels.

No significant difference in night sleep following cg knockdown using either RNAi construct. Regarding the work by Ceriani and colleagues Depetris-Chauvin et al. Yet importantly, they also show that action potential firing in adult PDF neurons constitutively expressing Kir2. Given this conclusion, we hope the reviewer understands that we are reticent to cite this manuscript as evidence that prolonged Kir2.

However, the same authors indeed later postulate that prolonged Kir2. Yet the data shown in this manuscript solely pertains to the function of the circadian oscillator, and there is no evidence presented of an effect of Kir2. Combined with data from Nitabach et al. We also note that other work from the Nitabach lab Figure 1, Wu et al.

Nonetheless, the reviewer is correct that there is evidence in the literature for a negative impact of constitutive expression of specific ion channels on the viability of certain neuronal subtypes. For example, Nadeau et al. We have therefore inserted the following text in the Discussion that cites both Nadeau et al. We hope the reviewer finds this alteration acceptable. In the figure legend of Figure 1—figure supplement 2K we have stated that two different chromosomal insertions of the same RNAi hairpin were used to knockdown cg These lines are also described in the Key Resources Table and the Materials and methods sections.

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication. We thank Jason Somers for technical support on infrared camera and DART system installation, Jack Humphrey for performing initial work on Neurocalcin knockdown flies, and Kyunghee Koh for helpful comments on the manuscript.

This article is distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use and redistribution provided that the original author and source are credited. Article citation count generated by polling the highest count across the following sources: Crossref , PubMed Central , Scopus. Cited 0 Views Annotations Open annotations. The current annotation count on this page is being calculated.

Cite this article as: eLife ;8:e doi: Figure 1 with 8 supplements see all. Download asset Open asset. Figure 2. Figure 3. Figure 4 with 2 supplements see all. Figure 5 with 2 supplements see all. Figure 6. Figure 7. Figure 8. Key resources table. How deeply does your mutant sleep? Genotype to phenotype: lessons from model organisms for human genetics B Lehner Nature Reviews Genetics 14 — ROMK1 Kir1. Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration G Tononi C Cirelli Neuron 81 — Hugo J Bellen.

K VijayRaghavan. Reviewer 1: The paper is well-constructed and well-written. Author response image 1. Author response image 2. Author response image 3. Author response image 4. Author response image 5. Author response image 6. Author response image 7. Author response image 8. Author response image 9. Author response image James Jepson. A two-part list of links to download the article, or parts of the article, in various formats.

Categories and tags Research Article Neuroscience sleep arousal neuronal calcium sensor circadian clock light Research organism D. Of interest.

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