JNK signaling triggers spermatogonial dedifferentiation during chronic stress to maintain the germline stem cell pool in the Drosophila testis

Herrera, Salvador C.; Bach, Erika A.

doi:10.7554/elife.36095

Cited by 32 publications

(47 citation statements)

References 42 publications

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“…The male and female germlines are maintained by proliferation of germline stem cells. These stem cells can be depleted by misexpression of differentiation factors in the stem cells or by starvation (Brawley and Matunis, 2004;Herrera and Bach, 2018;Kai and Spradling, 2004). Following these acute stresses, immediate stem cell daughters can de-differentiate back into stem cells to repopulate the stem cell compartment (Fig.…”

Section: The Germlinementioning

confidence: 99%

Model systems for regeneration: Drosophila

2020

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Drosophila melanogaster has historically been a workhorse model organism for studying developmental biology. In addition, Drosophila is an excellent model for studying how damaged tissues and organs can regenerate. Recently, new precision approaches that enable both highly targeted injury and genetic manipulation have accelerated progress in this field. Here, we highlight these techniques and review examples of recently discovered mechanisms that regulate regeneration in Drosophila larval and adult tissues. We also discuss how, by applying these powerful approaches, studies of Drosophila can continue to guide the future of regeneration research.

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Section: The Germlinementioning

confidence: 99%

Model systems for regeneration: Drosophila

2020

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“…Protein refeeding activates JNK signaling in germline and cyst cell lineage 9 . While JNK signaling activation in germline is required for de-differentiation of spermatogonia to GSCs, the role of JNK signaling hyperactivation in cyst lineage is unknown.…”

Section: Resultsmentioning

confidence: 99%

“…Starvation-induced spermatogonia death is triggered by the apoptosis of the surrounding somatic cyst cells 3 , which enclose the germ cells to regulate their self-renewal, proliferation and differentiation 4 – 8 . Protein resupply recovers GSC numbers and division, at least in part due to JNK-mediated de-differentiaion of spermatogonia to GSCs 9 . Somatic cyst cells are generated from division of cyst stem cells (CySCs).…”

Section: Introductionmentioning

confidence: 99%

Upregulated TNF/Eiger signaling mediates stem cell recovery and tissue homeostasis during nutrient resupply in Drosophila testis

Chang

Huang

et al. 2020

Sci Rep

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Stem cell activity and cell differentiation is robustly influenced by the nutrient availability in the gonads. The signal that connects nutrient availability to gonadal stem cell activity remains largely unknown. In this study, we show that tumor necrosis factor Eiger (Egr) is upregulated in testicular smooth muscles as a response to prolonged protein starvation in Drosophila testis. While Egr is not essential for starvation-induced changes in germline and somatic stem cell numbers, Egr and its receptor Grindelwald influence the recovery dynamics of somatic cyst stem cells (CySCs) upon protein refeeding. Moreover, Egr is also involved in the refeeding-induced, ectopic expression of the CySC self-renewal protein and the accumulation of early germ cells. Egr primarily acts through the Jun N-terminal kinase (JNK) signaling in Drosophila . We show that inhibition of JNK signaling in cyst cells suppresses the refeeding-induced abnormality in both somatic and germ cells. In conclusion, our study reveals both beneficial and detrimental effects of Egr upregulation in the recovery of stem cells and spermatogenesis from prolonged protein starvation.

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“…With regard to muscles, JNK function in Drosophila has been associated with myonuclear positioning and visceral muscle-intrinsic left-right asymmetry [18, 19] whereas Yki activity was described to be required for muscle growth during late pupal stages [20]. Both signaling pathways have also been implicated in dedifferentiation processes: active JNK in germ line cells [21] and Hippo (specifically, inactive Wts) in retinal cells [22]. We describe a novel, synergistic function of these two pathways in a specific type of muscle and connect them to lineage plasticity.…”

Section: Resultsmentioning

confidence: 99%

Yorkie and JNK revert syncytial muscles into myoblasts during Org-1 dependent lineage reprogramming

Schaub

Rose

Frasch

2019

Preprint

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SummaryLineage reprogramming has become a prominent focus in research since it was demonstrated that lineage restricted transcription factors can be used in vitro for direct reprogramming [1]. Recently, we reported that the ventral longitudinal musculature (VLM) of the adult Drosophila heart arises in vivo by direct lineage reprogramming from alary muscles (AM), a process which starts with dedifferentiation and fragmentation of syncytial alary muscles into mononucleate myoblasts. Central upstream activators of the genetic program regulating the development of VLMs from alary muscles are the T-box factor Org-1 (Drosophila Tbx1) and the LIM homeodomain factor Tup (Drosophila Islet1) [2]. However, the events downstream of Org-1 and Tup that exert dedifferentiation and fragmentation of alary muscles have been unknown. In the present report, we shed light on the initiation of this first step of transdifferentiation and show that AM lineage specific activation of Yorkie (Yki), the transcriptional co-activator of the transcription factor Scalloped (Sd), has a key role in initiating AM lineage reprogramming. An additional necessary input comes from active dJNK signaling, which contributes to the inactivation of the Hippo kinase cascade upstream of Yki and furthermore activates dJun. The synergistic activities of the Yki/Sd and dJun/dFos (AP-1) transcriptional activator complexes in the absence of Hippo activity initiate AM dedifferentiation and lead to the expression of Myc and piwi, which are crucial for different aspects of AM transdifferentiation. Our results provide new insights into the mechanisms that mediate muscle lineage plasticity during a cellular reprogramming process occurring in vivo.HighlightsDirect lineage reprogramming of alary muscles depends on Yorkie and JNKYorkie and JNK mediate reversal of syncytial muscle cell fateYki/Sd and AP-1 induce alary muscle dedifferentiation synergisticallyYki dependent Myc induces and Piwi mediates reprogramming of alary muscles

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JNK signaling triggers spermatogonial dedifferentiation during chronic stress to maintain the germline stem cell pool in the Drosophila testis

Cited by 32 publications

References 42 publications

Model systems for regeneration: Drosophila

Model systems for regeneration: Drosophila

Upregulated TNF/Eiger signaling mediates stem cell recovery and tissue homeostasis during nutrient resupply in Drosophila testis

Yorkie and JNK revert syncytial muscles into myoblasts during Org-1 dependent lineage reprogramming

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