The Conference on Computational Natural Language Learning (CoNLL) features a shared task, in which participants train and test their learning systems on the same data sets. In 2017, one of two tasks was devoted to learning dependency parsers for a large number of languages, in a realworld setting without any gold-standard annotation on input. All test sets followed a unified annotation scheme, namely that of Universal Dependencies. In this paper, we define the task and evaluation methodology, describe data preparation, report and analyze the main results, and provide a brief categorization of the different approaches of the participating systems.

Universal dependencies (UD) is a framework for morphosyntactic annotation of human language, which to date has been used to create treebanks for more than 100 languages. In this article, we outline the linguistic theory of the UD framework, which draws on a long tradition of typologically oriented grammatical theories. Grammatical relations between words are centrally used to explain how predicate–argument structures are encoded morphosyntactically in different languages while morphological features and part-of-speech classes give the properties of words. We argue that this theory is a good basis for cross-linguistically consistent annotation of typologically diverse languages in a way that supports computational natural language understanding as well as broader linguistic studies.

Impaired spermatogenesis and male infertility are common manifestations of mitochondrial diseases, but the underlying mechanisms are unclear. Here we show that mice deficient for PARL, the mitochondrial rhomboid protease, a recently reported model of Leigh syndrome, develop postpubertal testicular atrophy caused by arrested spermatogenesis and germ cell death independently of neurodegeneration. Genetic modifications of PINK1, PGAM5, and TTC19, three major substrates of PARL with important roles in mitochondrial homeostasis, do not reproduce or modify this phenotype. PARL deficiency in testis mitochondria leads to severe mitochondrial electron transfer chain defects, alterations in Coenzyme Q biosynthesis and redox status, and abrogates GPX4 expression specifically in spermatocytes leading to massive ferroptosis, an iron-dependent regulated cell death modality characterized by uncontrolled lipid peroxidation. Thus, mitochondrial defects can initiate ferroptosis in vivo in specific cell types by simultaneous effects on GPX4 and Coenzyme Q. These results highlight the importance of ferroptosis and cell-type specific downstream responses to mitochondrial deficits with respect to specific manifestations of mitochondrial diseases.

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