Biology subjects

Gunter, A.

Publications and source records attributed to Gunter, A..

4 recordsLinked to original sources

bioRxiv2024

Rapid wing size evolution in African fig flies (Zaprionus indianus) following temperate colonization

Invasive species often encounter novel selective pressures in their invaded range, and understanding their potential for rapid evolution is critical for developing effective management strategies. Zaprionus indianus is an invasive drosophilid native to Africa that reached Florida in 2005 and likely re-establishes temperate North American populations each year. We addressed two evolutionary questions in this system: first, do populations evolve phenotypic changes in the generations immediately following colonization of temperate environments? Second, does Z. indianus evolve directional phenotypic changes along a latitudinal cline? We established isofemale lines from wild collections across space and time and measured twelve ecologically relevant phenotypes, using a reference population as a control. Z. indianus evolved smaller wings following colonization, suggesting early colonizers have larger wings, but smaller wings are favorable after colonization. No other phenotypes changed significantly following colonization or across latitudes, but we did see significant post-colonization changes in principal components of all phenotypes. We documented substantial laboratory evolution and effects of the laboratory environment across multiple phenotypes, emphasizing the importance of controlling for both possibilities when conducting common garden studies. Our results demonstrate the potential for rapid adaptation in Z. indianus, which could contribute to its success and expansion throughout invaded ecosystems.

evolutionary biology↗

bioRxiv2024

Limited population structure but signals of recent selection in introduced African Fig Fly (Zaprionus indianus) in North America

Invasive species have devastating consequences for human health, food security, and the environment. Many invasive species adapt to new ecological niches following invasion, but little is known about the early steps of adaptation. Here we examine population genomics of a recently introduced drosophilid in North America, the African Fig Fly, Zaprionus indianus. This species is likely intolerant of subfreezing temperatures and recolonizes temperate environments yearly. We generated a new chromosome-level genome assembly for Z. indianus. Using resequencing of over 200 North American individuals collected over four years in temperate Virginia, plus a single collection from subtropical Florida, we tested for signatures of population structure and adaptation within invasive populations. We show founding populations are sometimes small and contain close genetic relatives, yet temporal population structure and differentiation of populations is mostly absent across North America. However, we identify two haplotypes that are differentiated between African and invasive populations and show signatures of selective sweeps. Both haplotypes contain genes in the cytochrome P450 pathway, indicating these sweeps may be related to pesticide resistance. X chromosome evolution in invasive populations is strikingly different from the autosomes, and a haplotype on the X chromosome that is highly differentiated between Virginia and Florida populations is a candidate for temperate adaptation. These results show that despite limited population structure, populations may rapidly evolve genetic differences early in an invasion. Further uncovering how these genomic regions influence invasive potential and success in new environments will advance our understanding of how organisms evolve in changing environments. Article SummaryInvasive species (organisms that have been moved outside their natural range by human activities) can cause problems for both humans and the environment. We studied the genomes of over 200 individuals of a newly invasive fruit fly in North America, the African Fig Fly. We found genetic evidence that these recently introduced flies may be evolving in their new environments, which could make them stronger competitors and more likely to become pests.

evolutionary biology↗

bioRxiv2024

Autosomal dominant Retinitis Pigmentosa caused by the rhodopsin isoleucine 255 deletion features rapid neuroretinal degeneration, decreased synaptic connectivity, and neuroinflammation.

Retinitis Pigmentosa (RP) is a group of inherited retinal diseases that initially affects rod photoreceptors and causes progressive vision loss and blindness. Mutations in rhodopsin (RHO) can cause both autosomal recessive (ar) and dominant (ad) forms of RP, yet, the underlying degenerative mechanisms remain largely unknown, rendering the disease untreatable. Here, we focus on an in-frame, 3-base pair deletion, eliminating the isoleucine residue at codon 255 (i.e., RHO{Delta}I255) and resulting in adRP. We generated a novel knock-in mouse homologous to the human RHO{Delta}I255 mutation. This new mouse model displays a severe disruption of photoreceptor structure and function, as is seen in human patients. Our results indicate that this form of RP is a systems disease of the neuroretina that also impacts neuronal connectivity of bipolar- and horizontal cells, initiates neuroinflammation, and reduces the structural and functional integrity of the retina. Typical for adRP, Rho{Delta}I255 mice exhibit primary rod photoreceptor loss, followed by secondary cone degeneration, rhodopsin protein (RHO) mislocalization, progressive shortening of outer segments (OS), and disorganized OS structures. Subsequently, increasing gliosis, morphologic abnormalities of the inner retina, and impaired cone-driven visual function developed. In adRP, a single mutated allele is sufficient to cause the disease, as confirmed here in Rho{Delta}I255/+ heterozygous animals, where most photoreceptors were lost within two months after birth. Compared to this, homozygous Rho{Delta}I255/{Delta}I255 mutants exhibit an accelerated onset and even faster progression of retinal degeneration. The degeneration of Rho{Delta}I255-mutant photoreceptors was linked to the activation of both caspase- and calpain-type proteases, as well as poly(ADP-ribose) polymerase (PARP), indicating a parallel execution of both apoptotic and non-apoptotic processes. In conclusion, our data indicate that this form of RP affects the neuroretina beyond photoreceptor cell loss sharing features typical for other degenerative central nervous systems diseases, an insight, which may bear critical impact to understand and eventually develop treatment for these currently untreatable forms of blindness. Author summaryDominant mutations in the human rhodopsin gene are among the most common causes for the blinding disease retinitis pigmentosa (RP). To date, the underlying pathophysiological mechanisms are still largely unknown and dominant RP remains untreatable. Here, we introduce a new knock-in mouse model carrying the dominant human Rho{Delta}I255 mutation. As in humans, the Rho{Delta}I255 mouse suffers from a rapid degeneration of rod photoreceptors followed by subsequent cell death of cone photoreceptors and complete loss of visual function. The new mouse model displays sign of neuroinflammation and the concomitant activation of both apoptotic and non-apoptotic cell death mechanisms. These results will likely stimulate further studies into the degenerative processes governing dominant RP and may facilitate future therapy development for inherited retinal diseases that are still untreatable to this day.

pathology↗

bioRxiv2021

Fine-tuned repression of Drp1 driven mitochondrial fission primes a slow cycling stem/progenitor-like state towards accelerating neoplastic transformation of keratinocytes

The opposing processes of mitochondrial fission and fusion are emerging as crucial regulators of stemness. Gene knockout of the master regulator of mitochondrial fission, Drp1, prevents neoplastic transformation. However, stem/progenitor cells maintaining repressed mitochondrial fission are primed for self-renewal and proliferation. Here, we demonstrate that only fine-tuned repression of Drp1 establishes a stem/progenitor-like state towards supporting carcinogen driven neoplastic transformation of keratinocytes, while more complete Drp1 repression prevents it. Only fine-tuned Drp1 repression maintains small networks of fused mitochondria to sustain a unique gene-expression profile with elevated stem/progenitor cell functional markers (Krt15, Sox2 etc) and their regulators (Cyclin E). Cells with such a mitochondria-primed state are slow cycling, susceptible to transformation, and when enriched by mild carcinogen exposure sustains elevated self-renewal/proliferation to form less differentiated tumors. Therefore, our data for the first time highlights a goldilocks level of Drp1 repression that supports stem/progenitor state dependent neoplastic transformation.

cell biology↗