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Primate inferotemporal cortex contains a coarse map of object space consisting of four networks, identified using functional imaging, electrophysiology and deep networks.

The inferotemporal (IT) cortex is responsible for object recognition, but it is unclear how the representation of visual objects is organized in this part of the brain. Areas that are selective for categories such as faces, bodies, and scenes have been found(1-5), but large parts of IT cortex lack any known specialization, raising the question of what general principle governs IT organization. Here we used functional MRI, microstimulation, electrophysiology, and deep networks to investigate the organization of macaque IT cortex. We built a low-dimensional object space to describe general objects using a feedforward deep neural network trained on object classification(6). Responses of IT cells to a large set of objects revealed that single IT cells project incoming objects onto specific axes of this space. Anatomically, cells were clustered into four networks according to the first two components of their preferred axes, forming a map of object space. This map was repeated across three hierarchical stages of increasing view invariance, and cells that comprised these maps collectively harboured sufficient coding capacity to approximately reconstruct objects. These results provide a unified picture of IT organization in which category-selective regions are part of a coarse map of object space whose dimensions can be extracted from a deep network.

Tandem repeat elements such as the diverse class of satellite repeats occupy large parts of eukaryotic chromosomes, mostly at centromeric, pericentromeric, telomeric and subtelomeric regions(1). However, some elements are located in euchromatic regions throughout the genome and have been hypothesized to regulate gene expression in cis by modulating local chromatin structure, or in trans via transcripts derived from the repeats(2-4). Here we show that a satellite repeat in the mosquito Aedes aegypti promotes sequence-specific gene silencing via the expression of two PIWI-interacting RNAs (piRNAs). Whereas satellite repeats and piRNA sequences generally evolve extremely quickly(5-7), this locus was conserved for approximately 200 million years, suggesting that it has a central function in mosquito biology. piRNA production commenced shortly after egg laying, and inactivation of the more abundant piRNA resulted in failure to degrade maternally deposited transcripts in the zygote and developmental arrest. Our results reveal a mechanism by which satellite repeats regulate global gene expression in trans via piRNA-mediated gene silencing that is essential for embryonic development.

A conserved satellite repeat in the mosquito Aedes aegypti encodes PIWI-interacting RNAs that promote sequence-specific gene silencing in trans and have an essential role in embryonic development.

The CRISPR system in bacteria and archaea provides adaptive immunity against mobile genetic elements. Type III CRISPR systems detect viral RNA, resulting in the activation of two regions of the Cas10 protein: an HD nuclease domain (which degrades viral DNA)(1,2) and a cyclase domain (which synthesizes cyclic oligoadenylates from ATP)(3-5). Cyclic oligoadenylates in turn activate defence enzymes with a CRISPR-associated Rossmann fold domain(6), sculpting a powerful antiviral response(7-10) that can drive viruses to extinction(7,8). Cyclic nucleotides are increasingly implicated in host-pathogen interactions(11-13). Here we identify a new family of viral anti-CRISPR (Acr) enzymes that rapidly degrade cyclic tetra-adenylate (cA(4)). The viral ring nuclease AcrIII-1 is widely distributed in archaeal and bacterial viruses and in proviruses. The enzyme uses a previously unknown fold to bind cA(4) specifically, and a conserved active site to rapidly cleave this signalling molecule, allowing viruses to neutralize the type III CRISPR defence system. The AcrIII-1 family has a broad host range, as it targets cA(4) signalling molecules rather than specific CRISPR effector proteins. Our findings highlight the crucial role of cyclic nucleotide signalling in the conflict between viruses and their hosts.