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Konecny, A.

Publications and source records attributed to Konecny, A..

3 recordsLinked to original sources

Incipient speciation, rapid expansion and repeated introgressive hybridization in an African Giant Shrew (Crocidura olivieri)

The African giant shrew (Crocidura olivieri) is one of the most widespread native small mammals in sub-Saharan Africa, occupying habitats ranging from humid tropical forests to arid Savanna. Its broad distribution, ecological diversity, and unresolved evolutionary relationships suggest a history of rapid diversification, yet the roles of hybridization and demographic expansion remain poorly understood. We combined genome-wide ddRAD and mitochondrial data from populations sampled across sub-Saharan Africa to reconstruct the evolutionary history of African giant shrews. We reveal extensive mitonuclear discordance across the clade and show that it reflects a complex history of repeated introgressive hybridization rather than a single evolutionary event. Genomic analyses resolve three major evolutionary lineages and identify four introgression events, including extensive bidirectional genome-wide introgression between the ancestors of the C. olivieri and arid adapted species followed by later unidirectional introgression associated with range expansion. Within the C. olivieri group, we identify five geographically structured lineages connected by ongoing gene flow, representing different stages of incipient speciation. Demographic analyses further reveal repeated population expansion during the Late Pleistocene and Early Holocene, with lineage-specific timing consistent with climatic fluctuations and a possible contribution of increasing human association. Our results identify repeated range expansion and hybridization as major drivers of diversification in African giant shrews and establish this system as a powerful model for studying the genomic processes underlying early speciation.

evolutionary biology↗

Human tissue-resident CD8 T cells contribute to trophoblast homeostasis in health and during acute inflammation

Previous studies have highlighted that some T cell subsets in tissues can provide signals to support tissue cell homeostasis and differentiation. If and how T cell-tissue cell signaling is altered in healthy compared to inflamed tissues is poorly understood. Here, we address if communication between human T cells and tissue cells changes from steady state to an acutely inflamed state in the human placenta. We used single cell analysis strategies to examine invasive cytotrophoblasts (iCTBs) and immune cells isolated from third trimester healthy and acutely inflamed human placentas. We performed cell communication analysis to predict cell-cell communication networks, and found evidence that iCTBs provided signals to support the recruitment of T cells, as well as the formation of tissue-resident memory CD8 T cells (Trm). In exchange, Trm provide signals to support iCTB homeostasis. During acute inflammation, iCTBs and macrophages underwent profound transcriptional changes, while most T cell subsets only underwent limited transcriptional changes. This was not due to T cell exhaustion or tolerance, as T cells were functionally intact. Cell communication analysis and validation at the protein level provide evidence that T cells can maintain their homeostatic support to iCTBs during acute inflammation.

immunology↗

TGF-β broadly modifies rather than specifically suppresses reactivated memory CD8 T cells in a dose-dependent manner

Transforming growth factor {beta} (TGF-{beta}) directly acts on naive, effector and memory T cells to control cell fate decisions, which was shown using genetic abrogation of TGF-{beta} signaling. TGF-{beta} availability is altered by infections and cancer, however the dose-dependent effects of TGF-{beta} on memory CD8 T cell (Tmem) reactivation are still poorly defined. We examined how activation and TGF-{beta} signals interact to shape the functional outcome of Tmem reactivation. We found that TGF-{beta} could suppress cytotoxicity in a manner that was inversely proportional to the strength of the activating TCR or pro-inflammatory signals. In contrast, even high doses of TGF-{beta} had a comparatively modest effect on IFN-{gamma} expression in the context of weak and strong reactivation signals. Since CD8 Tmem may not always receive TGF-{beta} signals concurrently with reactivation, we also explored whether the temporal order of reactivation versus TGF-{beta} signals is of importance. We found that exposure to TGF-{beta} prior to as well as after an activation event were both sufficient to reduce cytotoxic effector function. Concurrent ATAC-seq and RNA-seq analysis revealed that TGF-{beta} altered [~]10% of the regulatory elements induced by reactivation and also elicited transcriptional changes indicative of broadly modulated functional properties. We confirmed some changes on the protein level and found that TGF-{beta}-induced expression of CCR8 was inversely proportional to the strength of the reactivating TCR signal. Together, our data suggest that TGF-{beta} is not simply suppressing CD8 Tmem, but modifies functional and chemotactic properties in context of their reactivation signals and in a dose-dependent manner.

immunology↗