A method for generating a reporter cell line comprises culturing a cell line capable of undergoing two or more consecutive stages of differentiation and performing the targeted insertion of two or more secretable reporter genes into the genome of the cultured cell line to form edited cells. One or more first stage inserted secretable reporter genes are placed under control of promoters for genes canonically expressed during the first stage of differentiation, and one or more second stage inserted secretable reporter genes are placed under control of promoters for genes canonically expressed during the second stage of differentiation but not during the first stage of differentiation. Differentiation of the clonally expanded edited cells is then induced to the first stage of differentiation, thus inducing expression of the first stage inserted secretable reporter genes.

Methods and constructs for engineering circular RNA are disclosed. In some embodiments, the methods and constructs comprise a vector for making circular RNA, the vector comprising the following elements operably connected to each other and arranged in the following sequence: a.) a 5′ homology arm, b.) a 3′ group I intron fragment containing a 3′ splice site dinucleotide, c.) optionally, a 5′ spacer sequence, d.) a protein coding or noncoding region, e.) optionally, a 3′ spacer sequence, f) a 5′ Group I intron fragment containing a 5′ splice site dinucleotide, and g.) a 3′ homology arm, the vector allowing production of a circular RNA that is translatable or biologically active inside eukaryotic cells. Methods for purifying the circular RNA produced by the vector and the use of nucleoside modifications in circular RNA produced by the vector are also disclosed.

One variation of a method for producing a target compound includes: during an initial period, genetically modifying a population of insects to produce a target compound; during a growth period succeeding the initial period, cultivating the population of insects; during a treatment period succeeding the growth period, applying a dosage of a stressor to the population of insects, the stressor configured to trigger production of the target compound; in response to a proportion of the target compound within the population of insects exceeding a threshold proportion, harvesting the population of insects; homogenizing the population of insects to form a blend comprising the proportion of the target compound and a second proportion of a set of secondary components; and separating the proportion of the target compound from the second proportion of the set of secondary components for extraction of the proportion of the target compound from the blend.

The present invention relates to the field of fibrosis and inflammation and more particularly to the use of ADAM12 (A Disintegrin and Metalloproteinase 12) inhibitors to prevent or treat inflammation-induced fibrosis. The present invention also relates to the use of ADAM12 as a marker for inflammation-induced fibrosis and to the ablation of ADAM12 expressing cells as therapeutic approach to interfere with the development of pro-fibrotic cells.

Disclosed are non-naturally occurring zebrafish, such as transgenic zebrafish, which comprise a mutation in the rhodopsin (rho) gene. Also disclosed are methods of identifying compounds useful in treating retinal-specific defects and disorders, such as degeneration. Further disclosed are methods of identifying mutations in the rhodopsin gene that can cause retinal-specific defects.

Disclosed are non-naturally occurring zebrafish, such as transgenic zebrafish, which comprise a mutation in the rhodopsin (rho) gene. Also disclosed are methods of identifying compounds useful in treating retinal-specific defects and disorders, such as degeneration. Further disclosed are methods of identifying mutations in the rhodopsin gene that can cause retinal-specific defects.

The present invention provides polypeptides and nucleic acid molecules that are useful in identifying.

Provided are a method for constructing a mouse model with conditional knockout of the Tmem30a gene from a pancreatic cell and a use thereof. The construction method includes the steps of: constructing a homozygote mouse with conditional knockout of a Tmem30a gene, where both ends of one or more exons of the Tmem30a gene are inserted into directly arrayed loxp loci; and mating the mouse with a pancreatic cell specific transgenic mouse Ins2-Cre, thereby obtaining the mouse model with conditional knockout of the Tmem30a gene from the pancreatic cell. The mouse with conditional knockout of the Tmem30a gene from the pancreatic cell shows glucose intolerance and poor insulin sensitivity, and can be used as a diabetes research model.

A light-activated construct composed of two photoreceptive polypeptide domains connected to one another by a flexible linker is provided, as is a fusion protein containing the same and polynucleotides encoding said construct and fusion protein. Methods of making and using the light-activated construct and fusion protein are also provided.

This disclosure provides non-human animal models for age-related disorders and age-sensitive traits, particularly those caused by senescence-inducing stimuli, wherein the models comprise transgenes selectively expressed by senescent cells. The disclosure further provides methods for identifying therapeutic agents effective for treating or preventing age-related disorders and age-sensitive traits using the animal models, therapeutic agents identified using such methods, pharmaceutical compositions comprising the identified therapeutic agents, and methods of treating or preventing age-related disorders and age-sensitive traits.