PATZ1 is required for efficient HIV-1 infection

Aziati, Ishmael D.; Yoshida, Takeshi; Hamano, Akiko; Maeda, Kenjiro; Takeuchi, Hiroaki; Shoji, Yasuhiro

doi:10.1016/j.bbrc.2019.04.175

Cited by 5 publications

(2 citation statements)

References 26 publications

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“…BEAF32, dCTCF, Su(Hw), Zw5, GAF, CP190, MOD(MDG4)) 4,5 , later reports indicated additional insulators such as Pita and ZIPIC, the human ortholog of which is ZNF276 53,54 . Of note, several insulators such as dCTCF and Su(Hw) in Drosophila contain C2H2 zinc-finger domains implicated in DNA-binding and in particular, GAF, MOD(MDG4), and CP190 have BTB/POZ domains 4,55–57 involved in dimerization 58 and important for long-range interactions 59,60 , similar to PATZ1 in mammals 61 . Based on our analysis indicating the presence of PATZ1 at loops (Figures 2D and 2E), the reduction in looping interactions upon loss of PATZ1 (Figure 6 and S11), and the multimerization properties of CTCF in mammals 62 , the BTB/POZ domain of PATZ1 may be critical for homo/heterodimerization during loop formation.…”

Section: Discussionmentioning

confidence: 99%

Members of an array of zinc finger proteins specify distinctHoxchromatin boundaries

Ortabozkoyun

Huang

Cho

et al. 2023

Preprint

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CCCTC-binding factor (CTCF) and MAZ are recognized insulators required for shielding repressed posterior genes from active anterior genes within the Hox clusters during motor neuron (MN) differentiation. CTCF and MAZ interact independently with cohesin and regulate three-dimensional genome organization. Here, we followed cohesin re-location upon CTCF and MAZ depletion in mouse embryonic stem cells (mESCs) to identify novel insulators. Cohesin relocated to DNA motifs for various transcription factors, including PATZ1 and other zinc finger proteins (ZNFs). Moreover, PATZ1 and ZNFs co-localized with CTCF, MAZ, and cohesin with apparent overlapping specificity as dictated by the site to be insulated. Similar to CTCF and MAZ, PATZ1 interacted with RAD21. Patz1 KO mESCs exhibited altered global gene expression. While the absence of MAZ impacts anterior CTCF-boundaries as shown previously1, Patz1 KO led to de-repression of posterior Hox genes, resulting in cervicothoracic transformation of motor neuron (MN) fate during differentiation. These findings point to a varied, combinatorial binding of known and newly defined accessory factors as being critical for positional identity and cellular fate determination during differentiation.

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Section: Discussionmentioning

confidence: 99%

Members of an array of zinc finger proteins specify distinctHoxchromatin boundaries

Ortabozkoyun

Huang

Cho

et al. 2023

Preprint

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“…SLC25A42 fragments were cloned into pCSII‐EF‐IB‐RfA destination vectors using Gateway LR Clonase II enzyme mix (Invitrogen Corp.) to obtain pCSII‐EF‐IB‐SLC25A42. To obtain pCSII‐EF‐IB‐SLC25A42‐FLAG‐One‐STrEP (FOS) which is able to express FOS‐tag at the C‐terminus of SLC25A42, DNA fragments of SLC25A42 for pENTR‐SLC25A42‐FOS were amplified using pENTR‐SLC25A42‐FOS‐F and pENTR‐SLC25A42‐FOS‐R (see sequence described in Table 1) and cloned into pENTR‐FOS vectors 15 using Kpn I and Hind III restriction enzymes. SLC25A42‐FOS was cloned into pCSII‐EF‐IB using Gateway LR Clonase II enzyme mix.…”

Section: Methodsmentioning

confidence: 99%

Novel role of host protein SLC25A42 in the HIV‐1 reactivation of latent HIV‐1 provirus

Taga,

Takeuchi

2024

Microbiology and Immunology

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Despite the effectiveness of combination antiretroviral therapy, human immunodeficiency virus (HIV) infection remains incurable. To seek new strategies to overcome HIV type 1 (HIV‐1) latency, one of the major barriers to HIV elimination, it is crucial to better understand how this state is maintained. Here, by means of an RNA interference screen employing an HIV‐1 latency model using monocytic cell lines, we identified solute carrier family 25 member 42 (SLC25A42) as a potential host factor not previously known to affect HIV‐1 latency. SLC25A42 knockdown resulted in increased HIV‐1 expression, whereas forced expression of exogenous SLC25A42 suppressed it in SLC25A42‐depleted cells. SLC25A42 depletion increased HIV‐1 proviral transcriptional elongation but did not cause HIV‐1 activation in an HIV‐1 Tat‐depleted latency model. This suggests that the role of SLC25A42 in HIV‐1 transcription depends on HIV‐1 Tat. Chromatin immunoprecipitation‐qPCR analysis further revealed that SLC25A42 accumulated on or near the HIV‐1 5ʹ long terminal repeat promoter region of the HIV‐1 provirus, suggesting a possible role in regulating HIV‐1 Tat near this promoter region. These results indicate that SLC25A42 plays a novel role in HIV‐1 latency maintenance in monocytic HIV‐1 reservoirs.

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Identification and characterization of Stathmin 1 as a host factor involved in HIV-1 latency

Deletsu

Kitamura

Ishida

et al. 2021

Biochemical and Biophysical Research Communications

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PATZ1 is required for efficient HIV-1 infection

Cited by 5 publications

References 26 publications

Members of an array of zinc finger proteins specify distinctHoxchromatin boundaries

Members of an array of zinc finger proteins specify distinctHoxchromatin boundaries

Novel role of host protein SLC25A42 in the HIV‐1 reactivation of latent HIV‐1 provirus

Identification and characterization of Stathmin 1 as a host factor involved in HIV-1 latency

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