Chloroplast movement and positioning protein CHUP1 is required for focal immunity against Phytophthora infestans

When a plant detects a pathogen, chloroplasts terminate photosynthetic activity and uptake vital roles in the immune system to help stave off infection, including the production of defense hormone precursors and antimicrobial reactive oxygen species. Additionally, chloroplasts associate with the nucleus and produce greater numbers of tubular extensions called stromules during immune challenge. We previously showed that during infection by the potato blight pathogen Phytophthora infestans, chloroplasts accumulate at the pathogen haustoria, hyphal extensions that are accommodated within the host cell. However, the extent to which chloroplast positioning around haustoria, or at the nucleus, contributes to immunity during infection remains unknown. Here we show a striking increase in the susceptibility to P. infestans of Nicotiana benthamiana CRISPR knock-out lines lacking the chloroplast movement and anchoring gene, CHLOROPLAST UNUSUAL POSITIONING 1 (CHUP1). However, the positioning of chloroplasts around the haustorium or nucleus is not impaired in the absence of CHUP1. Further, loss of CHUP1 leads to an extreme clustering of chloroplasts around the nucleus in the presence and absence of infection, showing that greater chloroplast-nucleus association does not necessarily equate to more robust immunity. While plants lacking CHUP1 have reduced basal stromules, they are still able to induce stromules following immune stimulation, indicating that multiple populations of stromules exist. Lastly, we found that CHUP1 is required for proper deposition of callose - a cell wall material implicated in pathogen penetration resistance - around P. infestans haustorium, but not for other core immune processes. Our results implicate chloroplasts in plant focal immunity and point to a key role of CHUP1 in facilitating the deposition of defense material at the pathogen interface.

PSIX-30 Modulating action of fish oil on serum profiles of pigs exposed to prenatal inflammatory signals

Inflammatory signals elicited in response to stressors during gestation can affect fetal development and can have prolonged postnatal effects in the offspring. The objectives of the present study were to assess the effects of viral infection during gestation on nursed piglets, and to investigate possible modulating effects of fish oil. A total of 36 pigs were studied, distributed across three gilt treatment groups and sexes within treatment group. One-third of the piglets served as reference, being born from gilts that were not exposed to viral infection and receiving a non-supplemented diet. Another third of the piglets were born from gilts that were challenged with porcine reproductive and respiratory virus during the last third of gestation and receiving a non-supplemented diet. The remaining piglets were born from gilts that were challenged with the virus and were supplemented with fish oil (2.5 g of docosahexaenoic acid and eicosapentaeonic acid). All gilts received diets that met nutritional requirements during gestation and lactation (~90% corn and soybean meal). The piglets remained with the gilts and nursed until 22 d of age at which time blood was drawn and the levels of metabolic parameters were measured. The immune challenge during gestation had a significant effect on the level of globulin (P < 0.02). The globulin levels were higher in female piglets from gilts infected during gestation relative to control gilts. The blood level of triglycerides was similar between piglets from reference gilts and viral-infected gilts supplemented with fish oil, and lower than in piglets from non-supplemented infected gilts. Our results demonstrate that fish oil supplementation can modulate effects of infection during gestation on the piglet. This study is supported by USDA NIFA AFRI, grant number 2018-67015-27413.

Lymph node tissue homeostasis and adaptation to immune challenge resolved by fibroblast network mechanics

Emergent physical properties of tissues are not readily understood by reductionist studies of their constituent cells. Here, we show molecular signals controlling cellular physical properties, collectively determining tissue mechanics of lymph nodes, an immunologically-relevant, adult mammalian tissue. Lymph nodes paradoxically maintain robust tissue architecture in homeostasis yet are continually poised for extensive tissue expansion upon immune challenge. We find that following immune challenge, cytoskeletal mechanics of a cellular meshwork of fibroblasts determine tissue tension independently of extracellular matrix scaffolds. We determine that CLEC-2/podoplanin signalling regulates the cell surface mechanics of fibroblasts, permitting cell elongation and interdigitation through expedited access to plasma membrane reservoirs. Increased tissue tension through the stromal meshwork gates the initiation of fibroblast proliferation, restoring homeostatic cellular ratios and tissue structure through expansion.

Relish plays a dynamic role in the niche to modulate Drosophila blood progenitor homeostasis in development and infection

Immune challenges demand the gearing up of basal hematopoiesis to combat infection. Little is known about how during development, this switch is achieved to take care of the insult. Here, we show that the hematopoietic niche of the larval lymph gland of Drosophila senses immune challenge and reacts to it quickly through the nuclear factor-κB (NF-κB), Relish, a component of the immune deficiency (Imd) pathway. During development, Relish is triggered by ecdysone signaling in the hematopoietic niche to maintain the blood progenitors. Loss of Relish causes an alteration in the cytoskeletal architecture of the niche cells in a Jun Kinase dependent manner, resulting in the trapping of Hh implicated in progenitor maintenance. Notably, during infection, downregulation of Relish in the niche tilts the maintenance program towards precocious differentiation, thereby bolstering the cellular arm of the immune response.

Transgenerational Effects of Parental Diet on Offspring Development and Disease Resistance in Flies

The environmental conditions experienced by parents influence next generations, with the parental nutritional status playing an important role in shaping offspring phenotypes. Our understanding of transgenerational effects of parental diet on offspring pathogen resistance is, however, poorly documented. We manipulated the quality of parental diet (i.e., mother, father, or both) and measured effects on offspring development and survival after an immune challenge by septic infection. We used Bactrocera tryoni as host model infected with the pathogenic bacterium, Serratia marcescens. Our results showed no significant effect of maternal, or paternal, diet on offspring resistance. Interestingly, when the diet of both parents was manipulated, sons from parents fed either carbohydrate- or protein-biased diets had higher survival upon pathogen infection than sons from parents fed balanced diets. The quality of the parental diet had no effect on offspring developmental traits with the exception of egg hatching percentage which decreased when mothers were fed a protein-biased diet. Our results emphasised the complexity of nutritional transgenerational effects on offspring pathogen resistance and development.