Biology subjects

Lenhart, K. F.

Publications and source records attributed to Lenhart, K. F..

5 recordsLinked to original sources

bioRxiv2026

Regulated apoptosis is a conserved mechanism pausing female reproduction and establishes the sterile worker caste in the eusocial wasp, Polistes

Female reproduction is an energetically expensive process, so species evolve to balance survival with reproductive output. Many female organisms can temporarily pause their reproduction, including egg development, in response to physiological stress. The cellular mechanisms initiating and maintaining a stress-induced pause in oogenesis have been most extensively studied in Drosophila melanogaster. While the molecular control of paused oogenesis in response to starvation have been well characterized in flies, it remains unknown if these mechanisms are shared by other species with regulated pauses in oogenesis. Eusocial insects are characterized by a reproductive division of labor, with colonies of reproductive queens and sterile female workers. The social paper wasp, Polistes, has a dynamic dominance-based hierarchy for queen status. Worker Polistes are kept sterile by a combination of social and nutritional stressors. Here, we establish Polistes as a model to explore adult female reproductive plasticity. Through immunohistochemistry we have directly compared the Drosophila and Polistes ovarian structure and identified critical regions of the ovary in wasps that undergo regulated cell elimination during reproductive pause in flies. By comparing tissue structure, cell organization and rates of cell death between Polistes queens and workers we identified apoptosis as a key regulator maintaining worker sterility. Critically, this mechanism appears to be partially conserved with that in Drosophila. Finally, we find that changes in the timing and location of cell death in Polistes workers implicate oocyte identity and oocyte growth as additional potential regulators of temporary disruption of oogenesis. Summary StatementEstablishing the social paper wasp, Polistes, as a new model for female adult reproductive plasticity via temporary pausing of oogenesis in the sterile female workers.

developmental biology↗

bioRxiv2026

Somatic cells non-autonomously control germline incomplete cytokinesis through FGF signaling

Across species, germ cells divide and differentiate as interconnected units, termed cysts. These cysts are generated through reiterative rounds of mitosis followed by incomplete cytokinesis to generate stable ring canals (RCs). Despite the ubiquity of germ cell incomplete cytokinesis, it is still unclear how this program is mechanistically regulated across multiple cell cycles to retain integrity of the cyst. Here, by leveraging longitudinal live imaging of the Drosophila testis we have identified a critical, non-autonomous role for somatic support cells in maintenance of germline RC stability. We find that F-actin at RCs is stable throughout interphase but is dynamically disassembled and reassembled at each reiterative mitotic entrance and exit. Importantly, we find that somatic cells regulate the stability of interphase RC F-actin through the secreted growth factor, FGF. Genetic or pharmacological inhibition of FGF signaling induces disassembly of RC F-actin during interphase. Persistent clearance of F-actin from the RC leads to failure of incomplete cytokinesis and cyst abscission, suggesting that stable F-actin at RCs is required for the robust maintenance of incomplete cytokinesis through multiple rounds of germ cell divisions. Finally, we mechanistically link FGF signaling to germline activity of the non-receptor tyrosine kinase, Src64, which is known to regulate RC F-actin through Arp2/3. Taken together, we find a previously unappreciated role for somatic support cells in controlling an essential aspect of germ cell biology in the mitotically dividing spermatogonial pool. Summary StatementSomatic cells of the gonad secrete FGF ligand, Pyramus, which is required for maintenance of F-actin at germline ring canals and integrity of germline incomplete cytokinesis.

cell biology↗

bioRxiv2024

Conversion of somatic sex identity in the testis induces female-specific cellular behaviors in the soma and early oocyte specification in the germline

Establishment and maintenance of cellular sex identity is essential for reproduction. Critically, the sex identity of somatic and germline cells must correspond for sperm or oocytes to be produced, with mismatched identity causing infertility in all organisms from flies to humans. In the Drosophila testis, Chronologically inappropriate morphogenesis (Chinmo) is required for maintenance of adult male somatic identity. Loss of chinmo leads to progressive feminization of the male soma, including adoption of female-specific cell morphologies, tissue organization and gene expression. However, the degree to which this feminized soma in the male engages female-specific cellular behaviors or influences the associated XY germline is unknown. Using extended live imaging, we have visualized the process of male-to-female somatic sex conversion upon chinmo loss of function. We find that feminized soma in the testis engage cell behaviors characteristic of ovarian follicle cells (FCs), including female-specific incomplete cytokinesis, as early as one day of chinmo inhibition. In the ovary, FCs collectively migrate around the underlying germ cells to establish the elongated shape of the oocyte. Surprisingly, we find that FC-like soma in chinmo-depleted testes also engage this female-specific collective cell migration. Critically, migration of FC-like cells in the testis has the same molecular requirements as FC migration in the ovary. Depletion of the basement membrane protein Perlecan or adhesion protein Ecadherin significantly disrupts rotational migration in both the ovary and chinmo-depleted testes. Finally, we find that feminized soma non-autonomously alters sex identity of the associated XY germ cells, inducing expression of a protein required for early oocyte specification. Taken together, our work reveals a dramatic transformation of somatic cell behavior during the process of sex conversion and provides a powerful model to study soma-derived induction of oocyte identity.

developmental biology↗

bioRxiv2024

The Drosophila hematopoietic niche assembles through collective cell migration controlled by neighbor tissues and Slit-Robo signaling

Niches are often found in specific positions in tissues relative to the stem cells they support. Consistency of niche position suggests that placement is important for niche function. However, the complexity of most niches has precluded a thorough understanding of how their proper placement is established. To address this, we investigated the formation of a genetically tractable niche, the Drosophila Posterior Signaling Center (PSC), the assembly of which had not been previously explored. This niche controls hematopoietic progenitors of the lymph gland (LG). PSC cells were previously shown to be specified laterally in the embryo, but ultimately reside dorsally, at the LG posterior. Here, using live-imaging, we show that PSC cells migrate as a tight collective and associate with multiple tissues during their trajectory to the LG posterior. We find that Slit emanating from two extrinsic sources, visceral mesoderm and cardioblasts, is required for the PSC to remain a collective, and for its attachment to cardioblasts during migration. Without proper Slit-Robo signaling, PSC cells disperse, form aberrant contacts, and ultimately fail to reach their stereotypical position near progenitors. Our work characterizes a novel example of niche formation and identifies an extrinsic signaling relay that controls precise niche positioning. Impact StatementA new example of niche formation is provided which reveals the mode of niche cell migration, implicates extrinsic sources that deliver positional information, and uncovers the signaling pathway required for the precise, stereotypical positioning of the niche.

developmental biology↗

bioRxiv2023

Mating induces ecdysone signaling in the Drosophila testis niche disrupting somatic encystment of germ cells and stem cell cytokinesis

Germline maintenance relies on adult stem cells to continually replenish lost gametes over a lifetime and respond to external cues altering the demands on the tissue. Mating worsens germline homeostasis over time, yet a negative impact on stem cell behavior has not been explored. Using extended live imaging of the Drosophila testis stem cell niche, we find that short periods of mating in young males disrupts cytokinesis in germline stem cells (GSCs). This defect leads to failure of abscission, preventing release of differentiating cells from the niche. We find that GSC abscission failure is caused by increased ecdysone hormone signaling induced upon mating, which leads to disrupted somatic encystment of the germline. Abscission failure is rescued by isolating males from females but recurs with resumption of mating. Importantly, reiterative mating also leads to increased GSC loss, requiring increased restoration of stem cells via symmetric renewal and de-differentiation. Together, these results suggest a model whereby acute mating results in hormonal changes that negatively impact GSC cytokinesis but preserves the stem cell population. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=163 SRC="FIGDIR/small/562562v2_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@193d2f7org.highwire.dtl.DTLVardef@1ff602borg.highwire.dtl.DTLVardef@102cf0eorg.highwire.dtl.DTLVardef@167bd5f_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗