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DTSTAMP:20251216T100358
DTSTART;TZID=America/Detroit:20260122T090000
DTEND;TZID=America/Detroit:20260122T170000
SUMMARY:Exhibition:Tukilile Vaa
DESCRIPTION:Kaloki Nyamai is a multidisciplinary artist based in Nairobi. His practice explores Kenya's histories and collective memory\, blending Kamba traditions with contemporary narratives. Using acrylic paint\, rope\, photo transfers\, and stitched yarn\, his free-hanging immersive works blur the boundaries between painting\, sculpture\, and installation. For his U-M project\, Nyamai will present one large unstretched piece and two framed paintings at the Institute for the Humanities\, as well as a second free-hanging work at the U-M Museum of Art.\n\nThe physicality of his complex constructions inspire wonder in the viewer. The works are vast in scale\, embedded with stories\, where past and future merge both poetically and conceptually. In each composition\, the artist proposes a powerful alternative to the flatness of singular narratives of Kenyan history and identity presented as the definitive postcolonial account. He likens the formal act of stitching to symbolically unifying a wounded or fractured community.\n\nNyamai founded the Kamene Cultural & Research Center in Nairobi\, a creative and collaborative hub dedicated to the preservation\, promotion\, and innovation of African cultural practices.\n\nAbout the artist:\nKaloki Nyamai (*1985 in Kitui\, Kenya) is a multidisciplinary artist working with installation\, painting\, and sculpture based in Nairobi. From an early age\, his mother introduced him to painting and taught him to draw\, fostering an ever-lasting interest in art throughout his life. He often finds inspiration in his grandmother’s stories of the Kamba people\, a Bantu ethnic group of eastern Kenya. Using materials like acrylic paint\, sisal rope\, photo transfers\, and stitched yarn\, Nyamai’s free-hanging pieces evoke the healing of historical wounds and a collective yearning for renewal. His works blur the boundaries between painting\, sculpture\, and installation\, creating cohesive\, immersive experiences where past\, present\, and future converge poetically.\n\nNyamai studied Interior Design at the Buruburu Institute Of Fine Arts (BIFA) and then pursued painting after working in other creative fields. His large-scale paintings and mixed-media installations intricately explore historical narratives\, examining their resonance in the present. Nyamai has shown his work across the globe in solo exhibitions at the Norval Foundation\, Cape Town (2024)\; James Cohan Gallery\, New York (2024)\; Galerie Barbara Thumm\, Berlin (2023 and 2022)\; SEPTIEME Gallery\, Paris (2019)\, and other venues. In 2023\, he featured part of his series Dining in Chaos in the “Unlimited” section at Art Basel in Basel. He has participated in group exhibitions and biennials\, most recently at the Sharjah Biennial 16\, Sharjah (2025)\; The Völklinger Hütte\, Völklingen (2024)\; the Kenyan Pavilion at the Venice Biennale\, Venice (2022)\; and the Dakar Biennale (2022). His works are part of numerous private and institutional collections around the world\, such as the Dallas Art Museum\, the Southern African Foundation for Contemporary Art\, and the Arthur Primas Museum.
UID:142791-21891546@events.umich.edu
URL:https://events.umich.edu/event/142791
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Art,Exhibition,Humanities,Visual Arts
LOCATION:202 S. Thayer - Institute for the Humanities Gallery
CONTACT:
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BEGIN:VEVENT
DTSTAMP:20260113T150352
DTSTART;TZID=America/Detroit:20260122T093000
DTEND;TZID=America/Detroit:20260122T110000
SUMMARY:Workshop / Seminar:Dissertation Defense Seminar: Suji Ye
DESCRIPTION:Plants rely on a two-tiered immune system\, consisting of pattern-triggered immunity (PTI initiated by cell-surface pattern recognition receptors (PRRs) and effector-triggered immunity (ETI) activated by intracellular NOD-like (NLR) immune receptors. These two types of immunity are essential for protecting plants from pathogen invasion balancing growth and defense to maintain immune homeostasis. \n\nCalcium (Ca2+) is a secondary messenger that plays an essential role in plant immunity by transmitting immune signals from PRR and NLR receptors to downstream immune response upon pathogen perception and regulating processes such as transcriptional reprogramming\, reactive oxygen species production\, and kinase activation. However\, imbalanced Ca2+ signaling can induce autoimmunity\, causing cell death in plants.\n \nWe are interested in how Ca2+ signaling is integrated into a regulatory network that maintains immune homeostasis. In this thesis\, I characterized three closely related cyclic nucleotide-gated ion channels (CNGCs) acting as Ca2+ channels to suppress plant autoimmunity and regulate reproductive development. In Arabidopsis thaliana\, 20 CNGCs are classified into five groups (I\, II\, III\, IVa\, and IVb) based on sequence homology. Structurally\, Arabidopsis CNGCs contain six transmembrane domains\, a P-loop domain for ion selection\, a cyclic nucleotide-binding domain (CNBD)\, and a calmodulin-binding domain (CaMBD) for channel activity regulation. Our lab previously demonstrated that activation of CNGC19 and CNGC20\, upon phosphorylation by the receptor kinase BAK-to-life 2 (BTL2)\, induces massive intracellular Ca2+ influx\, leading to autoimmunity\, due to perturbation of the shared PRR-coreceptors BAK1/SERK4. In addition\, the chimeric CNGC11 and CNGC12\, which likely form an active calcium channel\, also cause autoimmunity. I systematically characterized CNGC11\, CNGC12\, and their closest homolog CNGC3 by generating single\, double\, and triple mutants with CRISPR-Cas gene editing. Importantly\, neither CNGC3\, 11\, nor 12 single or double mutants altered plant growth and immune responses. However\, the cngc3/11/12 triple mutants exhibited growth defects with varying levels of cell death. In addition\, the cngc3 single mutants showed infertility\, with shorter siliques and fewer seeds\, despite normal stamen and pistil structures. Using an Agrobacterium-mediated VIGS (virus-induced gene silencing) approach\, I show that the EDS1(ENHANCED DISEASE SUSCEPTIBILITY 1)-PAD4 (PHYTOALEXIN DEFICIENT 4)-ADR1s (ACTIVATED DISEASE RESISTANCE 1) module\, which plays a central role in toll/interleukin-1 receptor NLR (TNL)-mediated immunity\, is essential for the RNAi-CNGC3/11/12-induced cell death. RNA-sequencing analysis further suggests the involvement of additional Ca2+ channels\, pumps\, and TIR-domain-containing proteins in cngc3/11/12 cell death.  These results suggest that the depletion of CNGC3\, 11\, and 12 activates additional Ca2+ channels\, which further activate the TIR-EDS1-PAD4-ADR1s module to induce cell death. \n\nCeramides are a class of sphingolipids known to induce programmed cell death in plants and animals with unclear mechanisms. Mutation of ceramide kinase ACD5\, which results in the accumulation of high levels of ceramides\, induces spontaneous cell death in plants. Using VIGS\, I found that RNAi-ACD5-induced cell death depends on the NLR SUMM2 and other components of the SUMM2 signaling pathway. In addition\, ceramide levels are elevated in autoimmune mutants when SUMM2 is activated. Furthermore\, ceramides activate the phosphatase activity of Protein Phosphatase 5 (PP5) and promote PP5 interaction with the co-chaperone protein HOP1\, which are essential for SUMM2 activation. Collectively\, our findings reveal a mechanism by which ceramides promote cell death in plants through activation of a phosphatase that subsequently activates NLR immune receptors.\n\nIn summary\, our studies underscore the importance of maintaining balanced Ca2+ signaling and ceramide levels for immune homeostasis in plants.
UID:143855-21894126@events.umich.edu
URL:https://events.umich.edu/event/143855
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns,Dissertation Defense
LOCATION:Biological Sciences Building - 1010
CONTACT:
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