Our ability to perceive sounds relies on tiny cells deep inside our ears which can convert vibrations into the electrical signals that our brain is able to decode. These ‘hair cells’ sport a small tuft of short fibers on one of their ends that can move in response to pressure waves. The large amount of energy required for this activity is provided by the cells’ mitochondria, the small internal compartments that act as cellular powerhouses. In fact, reducing mitochondrial function in hair cells can lead to hearing disorders.

Mitochondria are often depicted as being bean-like, but they can actually adopt different shapes based on the level of energy they need to produce. Despite this link between morphology and function, little is known about what mitochondria look like in hair cells. Filling this knowledge gap is necessary to understand how these structures support hair cells and healthy hearing.

To address this question, McQuate et al. turned to zebrafish, as these animals detect vibrations in water through easily accessible hair cells on their skin that work just like the ones in the mammalian ear. Obtaining and analysing series of 3D images from a high-resolution microscope revealed that hair cells are more densely populated with mitochondria than other cell types. Mitochondrial organisation was also strikingly different. The side of the cell that carries the hair-like structures featured many small mitochondria; however, on the opposite side, which is in contact with neurons, the mitochondria formed a single large network. The co-existence of different types of mitochondria within one cell is a novel concept.

Further experiments investigated how these mitochondrial characteristics were connected to hair cell activity. They showed that this organisation was established gradually as the cells aged, with cellular activity shaping the architecture (but not the total volume) of the mitochondria.

Overall, the work by McQuate et al. provides important information necessary to develop therapeutics for hearing disorders linked to mitochondrial dysfunction. However, by showing that various kind of mitochondria can be present within one cell, it should also inform studies beyond those that focus on hearing.

Mitochondria are essential subcellular organelles in nearly all eukaryotic cells, where they perform and regulate manifold functions, including ATP production, calcium buffering, apoptosis, metabolite generation, among others. These functions are influenced by a cell’s total mitochondrial volume, regulated by mitochondrial biogenesis (Jornayvaz and Shulman, 2010) and subsequent mitochondrial architecture, sculpted by mitochondrial fusion and fission (Picard et al., 2013). Mitochondrial fusion and elongated mitochondria are associated with heightened mitochondrial membrane potentials, increased ATP production, and improved calcium buffering (Picard et al., 2013; Szabadkai et al., 2006; Gomes et al., 2011). Meanwhile, mitochondrial fission and smaller mitochondria are associated with lower mitochondrial membrane potentials, lower ATP production, and apoptosis (Liu et al., 2020). The combination of these features produces an overall mitochondrial phenotype according to cellular need. Failure to achieve an appropriate mitochondrial phenotype results in a variety of pathologies, particularly in highly metabolically active cells such as those that are electrically excitable (Reddy et al., 2011).

Hair cells (HCs) in the peripheral auditory nervous system mediate hearing and balance. Deflection of the stereocilia bundle at the apical pole of the HC results in cation influx in a process known as mechanotransduction, and subsequent depolarization and calcium influx through voltage-gated calcium channels (cav1.3) results in glutamate release from ribbon synapses at the basolateral pole onto afferent neurons. HCs heavily depend on mitochondria to sustain energetic demands, with 75% of their ATP usage produced via oxidative phosphorylation (Puschner and Schacht, 1997). It is perhaps due to their high dependency on mitochondria that HCs are particularly susceptible to mitochondrial alterations; mitochondria are implicated in both hereditary and environmentally induced hearing loss, as well as aging (Kokotas et al., 2007; Someya and Prolla, 2010; Böttger and Schacht, 2013). Mutations in over 30 mitochondrial-associated genes result in hearing loss in humans. These include mutations in the gene opa1, necessary for mitochondrial fusion (Leruez et al., 2013; Liguori et al., 2008).

Mitochondria are implicated at both poles of healthy HCs. In rat cochlear inner HCs, apical mitochondria have been shown to buffer calcium influx during mechanotransduction (Beurg et al., 2010; Pickett et al., 2018). Meanwhile, in zebrafish lateral line HCs, basal mitochondrial calcium uptake is essential for regulating ribbon size (Wong et al., 2019). Mitochondria also play a role in HC vulnerability to aminoglycoside exposure. HCs that have been treated with neomycin demonstrate abnormal mitochondrial morphologies prior to other insults (Owens et al., 2007). Neomycin-induced HC death requires mitochondrial calcium uptake (Esterberg et al., 2014 and Esterberg et al., 2016), and HC sensitivity to neomycin increases with cumulative mitochondrial activity (Pickett et al., 2018). Similarly, calcium import into the mitochondria via the MCU has been implicated in noise-induced hearing loss (Wang et al., 2018), and related mitochondrial potentials are disrupted in aging (Perkins et al., 2020).

Given the known impact of mitochondrial structure on their function, understanding the detailed morphological characteristics of HC mitochondria is a necessary first step for interpreting how these morphologies intersect with HC physiology and vulnerability (Lesus et al., 2019). We hypothesized that HCs maintained their mitochondria in an optimal configuration dependent on mitochondrial fusion to sustain high metabolic demands. Here, we detailed the characteristics of mitochondria in the HCs of the zebrafish lateral line. The lateral line is composed of clusters of HCs and surrounding supporting cells (SCs) called neuromasts (NMs) found on the surface of the fish’s body and detects changes in water flow. This information is vital for schooling and feeding behaviors. Lateral line HCs are genetically and morphologically similar to the HCs located within the mammalian inner ear, but are more easily accessible to genetic manipulations and experimentations (Pickett and Raible, 2019; Sheets et al., 2021). As fluorescent markers lack the resolution to distinguish between individual organelles, we turned to serial block-face scanning electron microscopy (SBFSEM) to produce three-dimensional reconstructions of HCs and their mitochondria with ultrastructural resolution. Over the course of this study, we reconstructed 5908 individual mitochondria from 162 different cells (16 NMs, 10 fish, Table 1). We demonstrated that zebrafish lateral line HCs had a mitochondrial phenotype distinct from SCs. This phenotype included a high total mitochondrial volume, and a particular architecture, with large, highly networked mitochondria at the basolateral pole near the synaptic ribbons, and smaller mitochondria positioned apically. This phenotype developed with HC maturation and was dependent on mechanotransduction and synaptic activity. Overall, our results demonstrate that HCs developed a highly specialized mitochondrial architecture sculpted by cell activity, which may explain their sensitivity to mitochondrial perturbation. Furthermore, the SBF datasets for each of the NMs used in this study have been made openly available, providing a comprehensive resource for further studying lateral line HCs and their organelles at the ultrastructural level.

Although mitochondria have long been known to be essential for HC function, a three-dimensional ultrastructural understanding of HC mitochondrial architecture, and its relationship to cell function, remained understudied. We used SBFSEM to describe an HC-specific mitochondrial phenotype characterized by (1) high mitochondrial volume and (2) a particular mitochondrial architecture, consisting of small mitochondria apically and large, networked mitochondria (max mito) near the synaptic ribbons. There are several caveats to using SBFSEM to study mitochondrial architecture. Although it is essential for resolving individual mitochondria, SBF requires fixed tissue, providing only a snapshot of the live mitochondrial dynamics that underlie the observed architecture. In addition, the laborious nature of the reconstructions precludes multiple replicates. However, we found no significant differences between HCs from different NMs and from different 5–6 dpf WT fish (65 HCs, 5 NMs from 3 fish), giving us confidence that our data reflect the greater population.

We found that lateral line HCs contain about 40 mitochondria in total. While this is over twice the number found in the surrounding SCs, it is notably on the smaller scale compared with numbers reported for other cell types, where estimates range from hundreds to thousands (Robin and Wong, 1988; Smith and Ord, 1983). We note these estimates were made from micrographs or measurements of mtDNA, which can vary widely. There are few studies that have similar complete reconstructions of total mitochondria in cells using high-resolution methodologies. A recent study indicates that there are nearly 500 mitochondria found in a primate cone photoreceptor after SBFSEM reconstruction (Hayes et al., 2021). Another recent study Liu et al., 2022 used SBFSEM to reconstruct mitochondria from mammalian cochlear HCs and estimated mitochondria numbered into the thousands. A better established measurement for comparison is mitochondrial volume as a fraction of the total cell volume (Posakony et al., 1977). Our measured ratio of mitochondrial volume to total cell volume in HCs (~7%, Figure 1H) is consistent with another recent study of mouse outer HCs that used EM tomography and estimated mitochondrial volume about 10% of cytoplasmic volume (Perkins et al., 2020). These numbers are also in alignment with SBFSEM reconstruction of neurons and glia in rat cortex, with mitochondrial volumes to cell volumes of 6–10% (Calì et al., 2019), though unfortunately mitochondrial number was not reported in this study.

We find distinct mitochondrial architecture along the HC apicobasal axis. At the HC apical pole, we find smaller mitochondria. In rat cochlear HCs, apical mitochondria take up calcium during mechanotransduction (Beurg et al., 2010), contributing to robust calcium buffering mechanics to maintain cytoplasmic calcium concentrations that could otherwise affect mechanotransduction and adaptation (Ricci et al., 1998; Eatock et al., 1987). Calcium influx itself could also lead to the smaller size of apical mitochondria. In neurons, calcium has been reported to induce mitochondrial fission (Rintoul et al., 2003), and the fission regulator Drp1 is activated by calcium (Cribbs and Strack, 2007; Han et al., 2008; Cereghetti et al., 2008). As excess calcium uptake can lead to mitochondrial damage (Starkov et al., 2004), mitochondrial fission in this region might facilitate mitophagy and quality control (Pfluger et al., 2015; Twig et al., 2008). The small size may also provide increased efficiency in packing, helping to maintain distinct calcium pools in apical and basal compartments, as has been suggested for photoreceptor mitochondria (Giarmarco et al., 2017). Mitochondria in opa1 mutants, which are uniformly small, demonstrated reduced calcium buffering. This could be a result of their small size or diminished mitochondrial health from lack of fusion, preventing resource sharing and hence leading to depolarized potentials. However, we note that mutations in opa1 will have multiple effects on mitochondrial function in addition to changes in size that may also influence their ability to take up calcium.

At the basolateral pole, HCs contained large mitochondrial networks (max mito) associated with ribbon synapses. Synaptic transmission requires large energetic expenditures (Li and Sheng, 2022). The proximity of the networked mitochondria to the synaptic ribbons suggests these large mitochondria might serve as active metabolic support. Mitochondrial fusion boosts oxidative phosphorylation and sharing of mitochondrial resources (Picard et al., 2013), indicating that the mitochondrial networks we observe would be particularly well-suited for this purpose. Synaptic mitochondria have been shown to take up calcium that enters through L-type CaV1.3 calcium channels, and disrupting this mitochondrial calcium uptake deregulated synaptic transmission (Wong et al., 2019). Larger mitochondria also have greater capacity to take up calcium (Kowaltowski et al., 2019; Szabadkai et al., 2006). As mitochondrial calcium uptake stimulates ATP production, interactions between mitochondrial fusion and synapse activity would be well-tuned to the cell’s energetic demands.

Our findings show that neither proper mechanotransduction nor synaptic activity is necessary for the growth in mitochondrial volume during HC maturation. This is surprising, given that HCs rely on oxidative phosphorylation for 75% of their metabolic needs (Puschner and Schacht, 1997), and changes in metabolic activity is a primary driver for mitochondrial biogenesis in many tissues (Jornayvaz and Shulman, 2010). Moreover, the role of calcium influx stimulating mitochondrial biogenesis in many other electrically active cell types, such as skeletal muscle and cardiomyocytes, is well established (Ojuka et al., 2002; Chin, 2004). We note that cdh23 mutations used to disrupt mechanotransduction still exhibit low levels of spontaneous synaptic release (Trapani and Nicolson, 2011) and cannot rule out the possibility that this residual activity might be sufficient to promote biogenesis. However, we can conclude that the growth of the mitochondrial volume is not regulated by overall activity levels. Additionally, we found that disrupting the mitochondrial architecture with a mutation in opa1 has no effect on the total mitochondrial volume. These fragmented mitochondria demonstrated depolarized potentials and decreased calcium uptake, likely associated with reduced ATP production. Together, these results suggest that the developmental increase in mitochondrial biogenesis is robust to changes in metabolic demands.

As the youngest HCs have a total mitochondrial volume similar to that of peripheral SCs, which serve as HC progenitors (Thomas and Raible, 2019), we suggest that the increase in mitochondrial volume is not linked to initial cell fate specification. Supporting this, the total mitochondrial volume increases gradually as HCs mature. This developmental mitochondrial growth is not driven by changes in cell volume, as described in other cell types (Rafelski et al., 2012; Miettinen and Björklund, 2017). Instead, it must be a product of different, ongoing pathways. One possibility may include the sirtuin deacetylases (SIRTs), key sensors of metabolism (Nogueiras et al., 2012) that can upregulate mitochondrial biogenesis through a series of parallel pathways (Yuan et al., 2016). In support of this, SIRT1 has been shown to be highly expressed in cochlear inner ear HCs (Xiong et al., 2014), and upregulation of SIRT1 pathways is protective against various modes of HC death (Zhan et al., 2021; Liang et al., 2021). The steady expansion of mitochondrial volume suggests these biogenesis-promoting pathways outweigh mitophagy and quality control. Such high mitochondrial volumes may produce dangerous reactive oxygen species (ROS) levels as a by-product of oxidative phosphorylation (Zhu et al., 2013). Therefore, the high mitochondrial volume might render HCs vulnerable to outside stresses that would additionally increase intracellular ROS. The observed mitochondrial networks might also in part counteract this vulnerability. Promoting mitochondrial fusion is protective against starvation-mediated apoptosis (Gomes et al., 2011) and SIRTs also regulate mitochondrial fusion (Uddin et al., 2021). SIRT3, located to mitochondria, has been implicated in counteracting age-related hearing loss and noise-induced damage (Someya and Prolla, 2010; Brown et al., 2014; Patel et al., 2020).

We found that mechanotransduction, while having little effect on mitochondrial biogenesis, was necessary for mitochondrial architecture. The clustered position of mechanotransduction mutants about midway within the mitochondrial UMAP trajectory (Figure 8) suggests a state of incomplete development where cells are unable to progress further. Lack of mechanotransduction resulted in fewer, larger, uniformly sized mitochondria. This is consistent with a model where apical calcium through mechanotransduction channels promotes mitochondrial fission. Mitochondria in mechanotransduction mutants also did not form basolateral networks localizing to synaptic ribbons. The fact that interference with mechanotransduction has effects on both formation of small mitochondria and localization of large, single networks suggests complex regulation of mitochondrial morphology.

By contrast, basal calcium entry associated with synaptic transmission is necessary for progressive growth of basal mitochondrial networks, but not formation of smaller apical mitochondria, which rapidly grew in number in cav1.3a mutants. In UMAP space, cav1.3a mutants intersperse with younger WT HCs, but segregate from mature HCs (Figure 8). Previous work (Trapani and Nicolson, 2011) has shown that cav1.3a mutants demonstrate reduced microphonic potentials, reflecting decreased mechanotransduction. If calcium influx drives apical mitochondrial fission, it is present at a level enough to do so in these mutants. Basal mitochondria take up calcium during synaptic transmission (Wong et al., 2019). This suggests a paradox where calcium might promote both mitochondrial fission apically and fusion basally. However, synaptic transmission requires large energy expenditures in addition to calcium regulation, and these demands may instead drive mitochondrial fusion into basal networks. Understanding the paradoxical effects of HC activity influencing both the formation of smaller apical mitochondria and larger basal networks will require additional study.

We find that altering calcium entry and synaptic transmission also altered ribbon size and morphology. These results compare with previous work showing that cav1.3a mutant HCs have enlarged ribbons (Sheets et al., 2012). Wong et al., 2019 demonstrated that blocking mitochondrial calcium entry also resulted in larger ribbons, a phenotype mimicked by altering NAD⁺/NADH ratios. While both of these studies showed larger ribbons after manipulating calcium and mitochondrial function, we observed cav1.3a mutant ribbons to be on average smaller than WT, but frequently found in clusters. We believe this discrepancy might be accounted for by the fact that the smaller ribbons we found in clusters at the EM level would appear to be larger single ribbons using fluorescence light microscopy methods employed in these previous studies. We also used strict structural parameters to define ribbons, which might account for differences in observed ribbon numbers and their locations as seen in fluorescence (Wong et al., 2019).

Not all HCs within zebrafish NMs are synaptically active, with active HCs tending to be younger cells on the NM periphery (Zhang et al., 2018; Wong et al., 2019; Lukasz et al., 2022). This is interesting, considering that we find the largest mitochondrial networks in more mature HCs. This discrepancy might be explained by considering that the initial onset of calcium entry associated with synaptic transmission might be sufficient to drive mitochondrial fusion, and that basolateral mitochondria remain networked regardless of whether the HC returns to a synaptically silent state during maturation.

Overall, our study provides a high-resolution, three-dimensional picture of zebrafish HC mitochondria, and demonstrates that through mechanotransduction and synaptic activity, these cells develop a finely tuned mitochondrial phenotype reflective of their function. This HC phenotype, through its high mitochondrial volume and large, appropriately positioned networked mitochondria, might be necessary to support high metabolic demands, but could also increase vulnerability to small fluctuations in intracellular ROS. Disruption of this phenotype could lead to improper HC physiology. Thus, it is critical that future studies take into account the high specificity with which HCs regulate their mitochondria.

The SBFSEM data volumes for the sixteen different NMs used in this manuscript, including WT and mutants, are publicly available at webKnossos (http://demo.webknossos.org/), searchable by the dataset name indicated in the relevant source data.

1. 1. McQuate AM
   2. Knecht S
   3. Raible D

   (2023) Webknossos

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   2. Knecht S
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   3. Raible D

   (2023) Webknossos

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Author details

1. Andrea McQuate

   1. Department of Biological Structure, University of Washington, Seattle, United States
   2. Department of Otolaryngology-HNS, University of Washington, Seattle, United States

   Contribution

   Conceptualization, Data curation, Formal analysis, Funding acquisition, Investigation, Methodology, Writing – original draft, Project administration

   For correspondence

   amcquate@uw.edu

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0002-2052-2004

2. Sharmon Knecht

   Department of Biological Structure, University of Washington, Seattle, United States

   Contribution

   Resources

   Competing interests

   No competing interests declared

3. David W Raible

   1. Department of Biological Structure, University of Washington, Seattle, United States
   2. Department of Otolaryngology-HNS, University of Washington, Seattle, United States

   Contribution

   Conceptualization, Resources, Data curation, Formal analysis, Supervision, Funding acquisition, Investigation, Methodology, Project administration, Writing - review and editing

   For correspondence

   draible@uw.edu

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0002-5342-5841

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