Abstract:The roundworm C. elegans transiently arrests larval development to survive extended starvation (1), but such early-life starvation reduces reproductive success (2, 3). Maternal dietary restriction (DR) buffers progeny from starvation, increasing reproductive success (4). It is unknown why early-life starvation decreases reproductive success and how maternal diet modifies this process. We show here that extended starvation in first-stage (L1) larvae followed 15 by unrestricted feeding results in a variety of abnormalities in the reproductive system, including glp-1/Notch-sensitive germ-cell tumors and uterine masses that express neuronal and epidermal markers. We found that maternal DR reduces the penetrance of starvation-induced abnormalities, including tumors. Furthermore, we show that maternal DR reduces insulin/IGF signaling (IIS) in progeny, and that daf-16/FoxO and skn-1/Nrf, transcriptional effectors of IIS, are required in 20 progeny for maternal DR to suppress abnormalities. daf-16/FoxO activity in somatic tissues is All rights reserved. No reuse allowed without permission.was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.The copyright holder for this preprint (which . http://dx.doi.org/10.1101/342956 doi: bioRxiv preprint first posted online Jun. 8, 2018; 2 sufficient to suppress starvation-induced abnormalities, suggesting cell-nonautonomous regulation of reproductive system development. This work reveals complex inter-and intragenerational effects of nutrient availability mediated by IIS with consequences on developmental integrity and reproductive success. One Sentence Summary: Intergenerational effects of diet on IIS 5Main Text: To determine how extended larval starvation compromises reproductive success, we compared early adult worms starved for 8 days as L1-stage larvae to control adults that were starved briefly, hereafter referred to as "starved" and "control", respectively. Approximately half of the starved worms displayed prominent abnormalities in their reproductive system despite being well fed after the starvation period (Fig. 1A-C). These abnormalities were highly variable, 10 both among worms and between gonads in an individual worm. The most common abnormalities fell on a spectrum ranging from gonads enlarged with proliferative germ cell nuclei (detected as 5-uterine masses were disorganized and appeared to contain differentiated cells. Indeed, the majority of uterine masses expressed elt-1 and unc-119 reporter genes, embryonic markers of epidermis and neurons, confirming somatic differentiation ( Fig. 1D and E). We observed similar abnormalities in three wild isolates subjected to 8 d L1 starvation (Fig. S1), suggesting that these abnormalities were not an artifact of the laboratory strain. Individuals with abnormalities 20 produced smaller broods (Fig. 1F), consistent with developmental abnormalities limiting reproductive success.All rights reserved. No reuse allowed without permission.was not peer-reviewed...
Cells and organisms typically cannot survive in the absence of water. However, there are some notable exceptions, including animals such as nematodes, tardigrades, rotifers, and some arthropods. One class of proteins known to play a role in desiccation resistance is the late embryogenesis abundant (LEA) proteins. These largely disordered proteins protect plants and animals alike from desiccation. A multitude of studies have characterized stress-protective functions of LEA proteins in vitro and in heterologous systems. However, the extent to which LEA proteins exhibit the same functions in their native contexts in animals is unclear. Furthermore, nothing is known about the distribution of LEA proteins in multicellular organisms or tissue-specific requirements in conferring stress protection. To study the endogenous function of LEA proteins in an animal, we created a true null mutant of C. elegans LEA-1, as well as endogenous fluorescent reporters of the protein. We confirmed that C. elegans lacking LEA-1 are sensitive to desiccation. LEA-1 mutant animals were also sensitive to heat and osmotic stress and were prone to protein aggregation. During desiccation, LEA-1 expression increased and became more widespread throughout the body. LEA-1 was required at high levels in body wall muscle for animals to survive desiccation and osmotic stress. We identified minimal motifs within LEA-1 that are sufficient to increase desiccation survival of E. coli. Our results provide insights into the endogenous functions and expression dynamics of an LEA protein in a multicellular animal. We show that LEA-1 buffers animals from a broad range of stresses. Our identification of functional motifs within the protein suggests the possibility of engineering LEA-1-derived peptides for desiccation protection.
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