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Burgin, G.

Publications and source records attributed to Burgin, G..

5 recordsLinked to original sources

A lectin receptor-like kinase controls self-pollen recognition in Phlox (Polemoniaceae)

Self-incompatibility (SI) describes a widespread collection of genetic mechanisms in flowering plants used to specifically recognize and reject self-pollen. These mechanisms are fundamental to plant sexual reproduction and offer valuable insight into the molecular basis of cell-cell communication and self-recognition more broadly. Here, we leverage an independent evolution of SI in the lineage containing Phlox (Polemoniaceae) to characterize a novel gene causing self-pollen recognition which we name Phlox drummondii Pistil Identity Receptor Kinase (PdPIRK). Recognition of self-pollen associates with a single genomic region containing the Phlox S-locus. We generate predictions regarding how S-loci must function and evolve to identify a single candidate gene within this S-associated region. This gene, PdPIRK, is highly and specifically expressed in the pistil and has exceptionally high polymorphism maintained by negative frequency dependent selection, two hallmarks of self-pollen recognition genes. Functional validation with gene silencing confirms that PdPIRK is necessary for self-incompatibility, and we further demonstrate allele specific activity, confirming its role in self-pollen recognition per se. PdPIRK encodes a G-type lectin receptor-like kinase, which is a member of the same gene family as SRK, the gene controlling self-pollen recognition in the distantly related Brassicaceae. Our findings suggest the presence of genetic constraints or paths of least resistance governing how S-loci evolve and add to our understanding of the diverse molecular mechanisms through which organisms achieve self-recognition.

plant biology↗

Mismatch between pollen and pistil size causes asymmetric mechanical reproductive isolation across Phlox species

In flowering plants, pollen-pistil interactions can serve as an important barrier to reproduction between species. As the last barrier to reproduction before fertilization, interactions between these reproductive organs are both complex and important for determining a suitable mate. Here, we test whether differences in style length generate a post-mating prezygotic mechanical barrier between five species of perennial Phlox wildflowers with geographically overlapping distributions. We perform controlled pairwise reciprocal crosses between three species with long styles and two species with short styles to assess crossing success (seed set). We find that heterospecific seed set is broadly reduced compared to conspecific cross success and reveal a striking asymmetry in heterospecific crosses between species with different style lengths. To determine the mechanism underlying this asymmetric reproductive isolating barrier we assess pollen tube growth in vitro and in vivo. We demonstrate that pollen tubes of short-styled species do not grow long enough to reach the ovaries of long-styled species. We find that short-styled species also have smaller pollen and that both within and between species pollen diameter is highly correlated with pollen tube length. Our results support the hypothesis that the small pollen of short-styled species lacks resources to grow pollen tubes long enough to access the ovaries of the long-styled species, resulting in an asymmetrical, mechanical barrier to reproduction. Such mechanisms, combined with additional pollen-pistil incompatibilities, may be particularly important for closely related species in geographic proximity that share pollinators.

evolutionary biology↗

Temporal single cell atlas of non-neuronal retinal cells reveals dynamic, coordinated multicellular responses to central nervous system injury

Non-neuronal cells play key roles in the complex cellular interplay that follows central nervous system (CNS) insult. To understand this interplay at a tissue level, we generated a single-cell atlas of immune, glial and retinal pigment epithelial cells from adult mouse retina before and at multiple time points after axonal transection (optic nerve crush; ONC), identifying rare and undescribed subsets, and delineating changes in cell composition, expression programs, and interactions. Computational analysis charted an inflammatory cascade after injury with three phases. The early phase consisted of reactivation of retinal macroglia and microglia, providing chemotactic signals for immune infiltration, concurrent with infiltration of CCR2+ monocytes from the circulation. In the second phase, these differentiated to macrophage subsets resembling resident border-associated macrophages. In parallel, a multicellular interferon program, likely driven by microglia-derived type-I interferon, was synchronously activated across resident glia, expanding beyond rare interferon-responding subsets of glia unexpectedly present in the naive retina. Our findings provide insights regarding post-injury CNS tissue dynamics and a framework to decipher cellular circuitry, spatial relationships and molecular interactions following tissue injury.

immunology↗

T helper cells modulate intestinal stem cell renewal and differentiation

In the small intestine, a cellular niche of diverse accessory cell types supports the rapid generation of mature epithelial cell types through self-renewal, proliferation, and differentiation of intestinal stem cells (ISCs). However, not much is known about interactions between immune cells and ISCs, and it is unclear if and how immune cell dynamics affect eventual ISC fate or the balance between self-renewal and differentiation. Here, we used single-cell RNA-seq (scRNA-Seq) of intestinal epithelial cells (IECs) to identify new mechanisms for ISC-immune cell interactions. Surprisingly, MHC class II (MHCII) is enriched in two distinct subsets of Lgr5+ crypt base columnar ISCs, which are also distinguished by higher proliferation rates. Using co-culture of T cells with intestinal organoids, cytokine stimulations, and in vivo mouse models, we confirm that CD4+ T helper (Th) cells communicate with ISCs and affect their differentiation, in a manner specific to the Th subtypes and their signature cytokines and dependent on MHCII expression by ISCs. Specific inducible knockout of MHCII in intestinal epithelial cells in mice in vivo results in expansion of the ISC pool. Mice lacking T cells have expanded ISC pools, whereas specific depletion of Treg cells in vivo results in substantial reduction of ISC numbers. Our findings show that interactions between Th cells and ISCs mediated via MHCII expressed in intestinal epithelial stem cells help orchestrate tissue-wide responses to external signals.

immunology↗