Methods and compositions for producing heme and treating sideroblastic anemia are disclosed.

Methods and compositions for producing heme and treating sideroblastic anemia are disclosed.

The present disclosure provides technologies for modulating microbiome of mammalian subjects (e.g., human subjects). The present disclosure, among others, provides therapeutic compositions and methods of using the same, wherein the therapeutic compositions comprising an engineered population of therapeutic bacteria that (i) are non-pathogenic and commensal in a subject to be administered; and (ii) are resistant to one or more target bacteriophages. In some embodiments, such therapeutic compositions can be useful for treatment of subjects suffering from or susceptible to a microbiome-dysfunction-associated disease, disorder, or condition (e.g., inflammatory bowel disease).

The present disclosure provides technologies for modulating microbiome of mammalian subjects (e.g., human subjects). The present disclosure, among others, provides therapeutic compositions and methods of using the same, wherein the therapeutic compositions comprising an engineered population of therapeutic bacteria that (i) are non-pathogenic and commensal in a subject to be administered; and (ii) are resistant to one or more target bacteriophages. In some embodiments, such therapeutic compositions can be useful for treatment of subjects suffering from or susceptible to a microbiome-dysfunction-associated disease, disorder, or condition (e.g., inflammatory bowel disease).

Disclosed herein are compositions and methods for modifying a bacterial population. In some embodiments, described herein is a bacteriophage comprising a first nucleic acid sequence encoding a first spacer sequence or a crRNA transcribed therefrom, wherein the first spacer sequence is complementary to a target nucleotide sequence from a target gene in a target bacterium, provided that the bacteriophage is rendered lytic.

Disclosed herein are compositions and methods for modifying a bacterial population. In some embodiments, described herein is a bacteriophage comprising a first nucleic acid sequence encoding a first spacer sequence or a crRNA transcribed therefrom, wherein the first spacer sequence is complementary to a target nucleotide sequence from a target gene in a target bacterium, provided that the bacteriophage is rendered lytic.

In certain embodiments a lentiviral vector for the treatment of Wiskott-Aldrich Syndrome (WAS) is provided. In certain embodiments the vector comprises an expression cassette comprising a nucleic acid construct comprising an effective fragment of the endogenous promoter of the WAS gene where said promoter has maximum length of 600 bp and contains the sequence of HS1pro, and a nucleic acid that encodes the Wiskott-Aldrich Syndrome protein (WASp) operably linked to the effective fragment of the endogenous promoter of the WAS gene.

In certain embodiments a lentiviral vector for the treatment of Wiskott-Aldrich Syndrome (WAS) is provided. In certain embodiments the vector comprises an expression cassette comprising a nucleic acid construct comprising an effective fragment of the endogenous promoter of the WAS gene where said promoter has maximum length of 600 bp and contains the sequence of HS1pro, and a nucleic acid that encodes the Wiskott-Aldrich Syndrome protein (WASp) operably linked to the effective fragment of the endogenous promoter of the WAS gene.

The invention relates to methods and compositions for treating or preventing an infection by E coli cells in human or animal subjects. The method comprises administering to the subject a plurality of transduction particles that encode a nuclease for targeting the genomes of B2 phylogroup E coli cells.

The invention relates to methods and compositions for treating or preventing an infection by E coli cells in human or animal subjects. The method comprises administering to the subject a plurality of transduction particles that encode a nuclease for targeting the genomes of B2 phylogroup E coli cells.